Nacle Physiology

Nacle Physiology
In the human body, there are two kidneys located behind the peritoneum, on either side of the spine at the lowest level of the ribcage [1]. Each
kidney is made up of millions of nephrons, which drain into a series of collecting ducts in the ureter and bladder. Each nephron consists of a
glomerulus, which is made up of a system of tiny blood vessels used to filter blood plasma. Each glomerulus is attached to an unbranched tubule [1]. In
the tubule, chemicals and water are either added or removed according to the body's needs. The products that are not needed are removed via urine. This
urine production is regulated in a variety of ways including the use of hormones and sympathetic nerve stimulation. These hormones, such as arginine
vasopressin ... Show more content on Helpwriting.net ...
Known as desmopressin, the drug can be taken regularly to treat pituitary and gestational DI [8]. As in nephrogenic and dipsogenic DI, the patient's
still produce vasopressin however has become resistant to it, so desmopressin cannot be used for treatment. In conclusion, urine production is
controlled and regulated by two hormones; arginine vasopressin and aldosterone. Both of these act to keep the level of urine production balanced with
fluid intake, however, problems can arise with these hormones which disrupt the balance leading to dehydration, polydipsia and nocturia. There are
however, options in order to treat the sufferers of all types of diabetes
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Gpr Structure
The understanding and studying of the GPCR structure is very important for designing the right drugs. Studies have shown that some of the GPCRs are
not pРѕtential drug targets because their physiological function cannot be related to disease. Such GPCRs include the sensРѕry (olfactory, taste)
receptРѕrs and thus, leave 369 GPCRs that are pРѕtential drug targets (Gloriam et al., 2007). 46 of these are being targeted successfully by drugs – the
rhodopsin–, secretin– and glutamate–like receptor families. ОІ–adrenergic, angiotensin II and vasopressin receptors are examples of GPCRs that are
lРѕcated in the membranes of cardiac cells and play key role in regulatiРѕn of the cardiac functiРѕn (for example, cardiac muscle contractility, blood
pressure, etc.).... Show more content on Helpwriting.net ...
Rimonabant is an agent that is an inverse agonist of the CB1 receptor but is known to have antagonist actions. As a result of those actions it reduces
obesity and smoking cessation but has side effects such as nausea, emesis, depression and anxiety (Despres et al., 2005) which were shown to be the
opposite effects of CB1 agonists. Therefore, novel drugs might be neutral antagonists and it has been suggested that they would not cause such side
effects. Laboratory studies provided evidence that inverse agonists (e.g. rimonabant) reduce fРѕРѕd intake and body weight, but cause gastrointestinal
side effects in rats, while neutral antagonists (e.g. AM6545, AM4113) also reduce fРѕРѕd intake and weight, but do not cause such adverse side effects
in the same animal models (Cluny et al., 2010; Cluny et al., 2011). Therefore, neutral antagonists are thought to be potential drugs for GPCRs, if acting
without any side effects (in the case of CB1 – provide action like rimonabant but do not cause gastrointestinal irritation or alter mood), but more
studies and experiments need to be done in order to provide evidence and release such drugs on the

A Short Note On Diabetes And Heart Failure Essay
пЃў –blockers in heart failure
Increased sympathetic activity has the ability to cause ventricular dysrhythmias following myocardial infarction [1]. –blockers as a class of drugs are
competitive antagonists which block the receptor sites of the endogenous hormones of the sympathetic nervous system: adrenaline and noradrenaline,
which can cause dysrhythmias.
Heart failure (HF) is failure of the heart muscle to sufficiently provide oxygenated blood to the organs of the body. This is a disease of the cardiac
muscle. This causes a reduction in the volume of blood the heart pumps and hence not enough blood to circulate and return to the heart and lungs.
This then results in the leakage of fluid, mainly water, from the capillary blood vessels which are responsible for the common symptoms of heart
failure; fatigue, shortness of breath and swelling [2]. Chronic Heart Failure (CHF) is a common clinical syndrome caused by Coronary Artery Diseases
(CAD), hypertension, valvular heart disease, and/or primary cardiomyopathy [3]. Ischemic Heart Disease (IHD) is mainly reduction of blood flow in
the coronary arteries to supply the heart with oxygen and nutrients due to narrowing of the coronary arteries normally due to the build up of fat
deposits in the blood vessel (atheroma).
Left ventricular dysfunction is often as a result of a myocardial infarction (acute) or hypertension (chronic) and this causes an upscale of the activities
of the sympathetic

Heart Failure (HF)
Heart failure (HF) is a complex syndrome in which structural or functional cardiac disorders impair the ability of one or both ventricles to fill with or
eject blood. HF is considered to be a chronic condition with periods of worsening symptoms that may require medical attention. It may present acutely
within just 24 hours in the form of pulmonary edema or even cardiogenic shock. To diagnose HF, three criteria need to be present: including shortness
of breath at rest or during exertion and/or fatigue, signs of fluid retention such as pulmonary congestion and/or ankle swelling, and objective evidence
of a decrease in myocardial performance at rest which is demonstrated using echocardiography.(1)
HF is currently one of the fastest growing problems ... Show more content on Helpwriting.net ...
In patients with symptomatic chronic HF who do not tolerate ACE inhibitors, angiotensin II type I receptor blockers (ARBs) can be used as an
alternative to improve morbidity and mortality. However, the higher rate of hypotension, renal dysfunction, and hyperkalaemia with such a
combination therapy warrants close monitoring of these parameters. As patients with end stage heart failure frequently show signs of fluid retention or
have a history of such, inhibitors of the renin–angiotensin system should be co–administered with diuretics most commonly loop diuretics, which
usually leads to rapid symptomatic improvement of dyspnea and exercise tolerance while lacking significant effects on survival. In addition to standard
treatment with ACE inhibitors and diuretics, patients with symptomatic stable systolic heart failure should be treated with b–adrenergic receptor
blockers unless there are contraindications. Additionally aldosterone receptor antagonists are recommended in addition to ACE inhibitors, b–adrenergic
receptor blockers, and diuretics, unless contraindicated.

Heart Failure: A Case Study
INTRODUCTION
Heart failure (HF) is a multifaceted clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of
the ventricle to fill with or eject blood.1 Heart failure is increasing in incidence, with 1 in 9 deaths in 2009 2.. Over 75% of existing and new cases
occurred in individuals greater than 65 years of age, less than 1% in individuals below 60 years and nearly 10% in those over 80 years of age. HF
continues to be significant burdens to healthcare systems in the Western world with over 432 billion spent each year in the United States alone4.
In the two last decades the cause of HF has shifted: in the late 1970s, rheumatic valvular disease was the primary cause, nowadays the leading ... Show
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Although current therapeutic approaches to HF improve symptoms, they are palliative in the sense that they do not address the fundamental problem –
the loss of cardiac tissues. It is for this reason that stem cells have sparked intense interest. Stem cells by definition are cells that have the potential to
become any type of cell in the body, they can self–renew or multiply while maintaining the potential to develop into cells such as cells blood, heart,
bones, skin, muscles, brain etc. According to some researches, stem cell–based therapies have the potential to dramatically transform the treatment and
prognosis of HF by achieving what would have been unthinkable only a few years ago. They also asserted that for the first time since cardiac
transplantation, a therapy is being developed to eliminate the underlying cause of HF, not just to achieve damage control. In 2001, the first study of
bone marrow cells in experimental myocardial infarction (MI) was published,9 within a year, this therapy had been applied in patients.10 In the
setting of HF, it took only three years from the first use of stem cells (skeletal myoblasts) in an animal model to the first use of these cells in

Controlled Release Nifedipine Case Summary
Nifedipine is a calcium channel blocker which can be used alone or in conjunction with other medications for treatment of angina and hypertension. It
decreases the contractility of the arterial smooth muscle as well as the subsequent vasoconstriction through inhibition of calcium ions influx through
the L–type calcium channels. As a result, the coronary and systemic arteries become dilated and the delivery of oxygen to the myocardial tissue is
increased. Furthermore, the total peripheral resistance is decreased as well as the systemic blood pressure and afterload. When being prescribed with
controlled release nifedipine, Mrs Luv would be advised to take great caution because she may be more sensitive to the effects of the drug because of
her age. She would be instructed to swallow the medication whole (no chewing, breaking or crushing the tablet) with a glass of water and not to
abruptly stop taking the medication without consultation with her physician. She would be informed that controlled release nifedipine may ... Show
more content on Helpwriting.net ...
First of all, her age is a concern as this dictates her ability to react to the drug which ultimately affects the effectiveness of the medication. Second, she
is pre–diabetic, hence we should be looking for an antihypertensive with a hypoglycaemic action to at least reduce the possibility of her having Type
II Diabetes Mellitus whilst managing her high blood pressure. Third, she has liver impairment and unfortunately, she is causing further liver damage
through her drinking habits. This presents a challenge to look for an antihypertensive drug which is the least hepatotoxic so as not to contribute to
the liver impairment she currently has. Finally, it is already established that Mrs Luv has poor compliance when it comes to her health. Therefore, a
medication with a frequency of once a day is better as it will be easier for her to

Study on Essential Hypertension
PRESENTATION BY:
GIZELLE WILKINSON
SUBJECT: ESSENTIAL HYPERTENSION
STUDENT NUMBER: M00037713
CLINICAL SCIENCES II
INTRODUCTION
Essential hypertension, otherwise known as primary or idiopathic hypertension, is a condition of raised blood pressure with no identifiable cause.
Secondary hypertension occurs when blood pressure elevation results from a specific and potentially treatable cause. These include renal diseases,
endocrine causes, congenital cardiovascular causes and pregnancy.
This study however, will focus on essential hypertension so as to avoid unnecessary confusion. Blood pressure is relative to each individual and tends
to vary markedly depending on height and weight. Levels of blood pressure ... Show more content on Helpwriting.net ...
In the arteries, there is thickening of each of the layers in the vessel wall, thus narrowing the lumen and reducing its effectiveness. A similar
development occurs in the arterioles causing increased rigidity of the walls thus reducing their ability to contract and expand. Hence the lumen size is
reduced. As a result, there is slowing down of the blood flow resulting in 'ischaemia' of cell tissue.
This then increases the pressure through the vessels and the left ventricular myocardium or heart muscle undergoes hypertrophy. Ischaemic heart
disease and left ventricular failure are common results of hypertension in this case.
Due to occurrence of the above, the blood vessel in the brain become more fragile and paves the way for haemorrhage. Damage to small blood vessels
within the cerebral hemispheres produce microscopic infarctions (localised necrotic areas) appearing as small areas of brain destruction that fill with

fluid, otherwise known as hypertensive lacunae.
In malignant hypertension the vessels undergo similar changes but more acutely. Therefore the damage is more severe, leading to actual cessation of
blood flow through the vessels. This results in multiple areas of tissue necrosis as in the glomeruli of the kidney.
As the glomeruli are part of the filtration system in the nephron of the kidney, damage can hinder removal of waste products, salt and water from the
blood stream. Progressive destruction of

Essay on Endothelium in Health and Disease
Investigation of the influence of the endothelium on the actions of acetylcholine and nitroprusside.
Results (a) Estimate the maximum responses (Emax) and EC50 values for phenylephrine with the two types of arterial ring. Put this data in a single,
self–explanatory table.
Table1. Emax and EC50 values for phenylephrine. Phenylephrine| Emax in grams tension| EC50 in nM| Endothelium intact| 2.2| 40| Endothelium
denuded| 2.9| 10|
(c) Estimate the EC50 values for the effects of acetylcholine and nitroprusside in both types of arterial ring, and present these in a table. Table 2. EC50
values for the effect of acetylcholine and nitroprusside. EC50 in nM| ... Show more content on Helpwriting.net ...
Shearing forces acting on the vascular endothelium generated by blood flow causes a release of calcium and subsequent cNOS (cyclic nitric oxide
synthase) activation. Therefore, increases in blood flow stimulate NO formation (flow–dependent NO formation). Nitric oxide then causes independent
vasodilation by inhibiting vasoconstrictor influences of phenylephrine and alters its potency and contractile effect. (Richard E. Klabunde. 2010)
However, it has a short half–life of only a few seconds. In endothelial denuded preparations there was no production of nitric oxide and subsequently no
flow dependent vasodilation occurred. So, without endothelium a response of phenylephrine is not inhibited and therefore it exhibits a higher
potency(lower EC50) and efficacy. f) Account for the response to acetylcholine in the two preparations. Which receptor(s) mediates the effects of
acetylcholine in the rings with and without endothelium? As shown in the table 2 the EC50 values of acetylcholine, calculated from the dose–response
curve, significantly differ from each other. In fact, in endothelium denuded rings acetylcholine caused no relaxation at all. Moreover, the prolonged
exposure to increasing concentrations had given some constriction. In human and animals 5 sub types of muscarinic receptors (M1–M5) have been
identified. In the particular case of human blood vessels, the M3 subtype seems to be prevalent on endothelial cells as

Marfan's Syndrome Essay
Marfan's syndrome is a rare hereditary disorder of the body's connective tissue. The phenotypic traits include being tall, abnormally long stretched
limbs and in the most severe cases the aorta can be prone to rupture and retinal detachment can occur [1]. Seventy five percent of cases for this
multisystem disorder are genetic and inherited in an autosomal dominant fashion (a child can inherit it from just one parent): 25% are sporadic where
neither parent has the syndrome [2]. Its prevalence is 1/5000 and of these affected individuals each has a 50% chance of passing on the mutated gene
to their offspring [3]. Marfan's syndrome is caused by mutations in the fibrillin–1 gene (FBN1) located on chromosome 15q21.1 [4]. Fibrillin is a large
glycoprotein... Show more content on Helpwriting.net ...
Two thirds (approximately 66%) of Marfan's syndrome sufferers experience problems in the cardiovascular system and have mitral valve prolapse;
where blood may flow back from the ventricles into the atrium in a process called mitral valve regurgitation. This may require valve repair or valve
replacement. If cardiac arrhythmias occurs – where the heartbeat becomes irregular – there is the risk of sudden death [2]. Thoracic aortic aneurysm is
also prevalent in Marfan's syndrome sufferers. This is a condition caused by the widening of the aorta due to weakness in the walls of the vessel.
Aneurysm can lead to rupture itself or to aortic dissection where the aorta wall tears thus allowing blood to flow between the layers of the blood
vessel walls. It can result in rupture or in a decrease in blood flow to the organs. This situation is very dangerous and is most likely to require heart
surgery or aortic replacement

High Blood Pressure Is The Resistance Of Blood Vessels
Blood pressure is the force exerted by the blood against the walls of blood vessels, and the magnitude of this force depends on the cardiac output
and the resistance of the blood vessels. When the systolic blood pressure (SBP) which is the pressure as the heart pumps blood around the body is
140 mm Hg or more, or a diastolic blood pressure (DBP) which is the pressure as the heart relaxes and refills with blood, is 90 mm Hg or more, and
the individual is taking antihypertensive medication, it is called Hypertension (Madhur, 2014). High blood pressure is a major risk factor for various
other illnesses and even death due to several cardiac and vascular diseases. It is assessed that about 54% of strokes, 47% of heart attacks, 75% of
hypertensive disease, 25% of other heart disease, 13.5% of all mortality, and 6% of morbidity are linked to Hypertension (Khraim & Pike, 2014).
Hypertension affects about 70 million adults in the United States. Only about half (52%) of people with hypertension have their blood pressure under
control. Nearly 1 in 3 American adults have prehypertension which means that blood pressure numbers are greater than usual, but not in the high blood
pressure range. Hypertension costs the country about $46 billion annually. This comprises the cost of health care services, drugs to treat hypertension,
and days of absence from work (CDC, 2015).
Pathophysiology of the disease
The pathogenesis of essential hypertension involves various elements and is extremely

Gymorphism In Gymnastics
Originating as a sporting scheme to enhance a male's performance within warfare, gymnastics has flourished into a sporting activity enjoyed by many
around the world. However, it was not until the 1800's when the Germans and Swedish developed the modern rules. Since gymnastics entered the
Olympic roster in 1896, the sport has developed into a professional sport characterised by agility, athleticism and small body size. Although this sport
is enjoyed by a variety of people around the globe, only a select few have the capabilities of becoming an elite gymnast. Over the past one hundred
years there have been little changes within the evolution of the human body, however the world has seen dramatic changes within the sporting world.
These changes... Show more content on Helpwriting.net ...
There are many theories presented on this debate yet there is limited scientific data confirming any theory. However all theories lead to a similar
conclusion, training is needed in order to see improvement and achieve success. The controversial side is whether genetics is a major factor,
numerous studies conducted lead to the scientifically proven fact that genetics determines your base level along with your physical peak. To test this,
scientists subjected untrained people to the same training regime in order to see their improvement levels. From this, it was plain to see that some
candidates saw great improvements whilst others saw little. Through further studies it was evident that those who were related saw similar results,
from this we are able to gather that genetics play a major part in you athletic improvement. Those who saw significant improvements were deemed as
high responders, whilst those who saw little are low responders. Athletes who compete at international level and achieve high results have been
recognised to be high responders along with completing an excessive training regime and hold a superior make–up. Although training may show
improvements without a good genetic make–up your chance of reaching a professional level is near

Current Treatments Targeting Raas And Its Effect On The...
CURRENT TREATMENTS TARGETING RAAS
Because the RAAS has such a profound effect on the increase of blood volume during HF, it is an excellent target for many therapeutic agents. Current
pharmacological treatments for HF that target the renin–angiotensin–aldosterone system include ACE inhibitors and Angiotensin II receptor blockers
(ARBs).
ACE inhibitors such as Captopril block activity of the enzyme ACE and therefore the conversion of angiotensin I to angiotensin II (the most bio active
product of the RAAS), thus inhibiting the actions of angiotensin II and leading to decreased aldosterone production, decrease blood volume and reduced
hypertension. ACE inhibitors also work to decrease fibroblast activity as a protective measure against remodelling of the left ventricle (19). Side
effects of ACE inhibitors include a dry cough due to the inhibition of bradykinin break down, hypotension and hyperkalemia (due to higher levels of
potassium reuptake). ACE inhibitors are currently one of the drugs of choice to treat patients with HF.
ARBs such as Lostaran compete with angiotensin II to bind to the AT1 receptors and prevent the systemic effects of increased levels of angiotensin II
in HF (23). This acts to prevent the blood pressure increasing effects of the RAAS. These drugs are generally better tolerated than ACE inhibitors and
they do not inhibit bradykinin breakdown so patients do not demonstrate the dry cough associated with ACE inhibitors. Side effects of angiotensin II
receptor

INTRODUCTION:- HISTORICAL BACKGROUND OF ANTIHYPERTENSIVE...
INTRODUCTION:– HISTORICAL BACKGROUND OF ANTIHYPERTENSIVE THERAPY Antihypertensive therapy with the conventional drugs
such as thiazide diuretics,beta –adrenoreceptor antagonists and Calcium channel antagonist (CCA ) based regimens can reduce the risk of stroke and
other cardiovascular events. The drugs used as first line therapy in both younger and elderly patients include the conventional drugs such as diuretics,
CCA or ACE inhibitors based regimens[6][7] ACE inhibitors such as Captopril and enalapril are used clinically for the treatment of hypertension and
congestive heart failure(CHF). Despite the fact that ACE inhibitors have met with a high degree of success, ACE is a nonspecific protease responsible
for degradation of bradykinin... Show more content on Helpwriting.net ...
So we got an idea to synthesize some new AT1 receptor antagonists which do not have these side effects. RENIN ANGIOTENSIN ALDOSTERONE
SYSTEM:– [13] The renin angiotensin system is one of the powerful regulators of blood pressure and volume homeostatis. Renin is a proleolytic
enzyme which is produced in the juxtaglomerular apparatus of the kidney. It acts on the angiotensinogen which is a–globulin produced by the liver.
Then there is a formation of Angiotensin 1 (decapeptide) Asp–Arg–Val–Tyr–Ile–His–Pro–Phe–His–Leu. Ang1 has little biological activity. Then
Angiotensin is produced when there is removal of the C –terminal dipeptide Histidyleucine from Ang 1 by the action of metalloprotease enzyme ACE
(Angiotensin converting enzyme) mainly present in lungs and Angiotensin II (1–8) is produced which is an octapeptide in regulating the
mineralocorticoids, it induces the sodium and water retention in the body. ANGIOTENSIN II RECEPTOR BLOCKERS:– Angiotensin II receptor
blockers (ARBs) (eg, valsartan, losartan, candesartan, telmisartan, tolmesartan, and irbesartan) act by selectively blocking the AT1 receptor, thereby
directly blocking the vasoconstrictor and growth effects of Ang II.[16] Selective blockade of the AT1 receptor has additional cardiovascular benefits
resulting in vasodilation, growth

Hypertension : High Blood Pressure
Hypertension is commonly known as high blood pressure. What does it mean to have high blood pressure? Blood pressure can be defined as the
amount of blood the heart pumps and the amount of resistance to blood flow in the arteries. It is when the systolic reading is greater than 140 and the
diastolic is greater than 90. Systolic is blood pressure when the heart contracts while diastolic is the time when the heart is relaxed. Primary care
physicians are accustomed to seeing cases of hypertension. However this common diagnosis can lead to more serious illnesses such as chronic kidney
disease, stroke, heart attack, aneurysm, peripheral artery disease, and even death (Tipton & Sullivan, 2014).
Hypertension usually occurs with no symptoms however its effects are seen in other serious diseases as mention previously. One way of knowing
whether a patient is suffering from high blood pressure is to have their blood pressure checked. Most severe cases of hypertension can cause
symptoms of severe headache, nausea or vomiting, confusion, vision changes, and nosebleeds. There are many reasons why a patient may have high
blood pressure. Eating a diet containing high levels of sodium is one cause. Others include drinking too much alcohol, smoking, obesity, and if a
person is more stressed or anxious. Medical history also plays a significant role in whether a person will suffer from hypertension. Histories of
diabetes or family history of high blood pressure are risk factors. Certain

Type 2 Diabetes Mellitus As A Disease State
Type 2 Diabetes Mellitus is a disease state which increases with age and targets many ethnicities and populations.1 Type 2 diabetes is not a
condition that an individual is born with, rather, it is a condition that is acquired later in life beginning as early in adolescence. The ethnicities in
which type 2 diabetes is most prevalent in are: Native Americans, Hispanic Americans, Asian Americans, African Americans, and Pacific Islanders.
Most cases of type 2 diabetes are associated with an obese and sedentary lifestyle meaning poor eating habits and lack of exercise. In the United
States, 11.3% of people 20 years old and over are diagnosed with type 2 diabetes. There are many risk factors in the development in type 2 diabetes,
these risk factors include but are not limited to: family history, obesity, chronic physical inactivity, race or ethnicity, history of glucose tolerance,
impaired fasting glucose, or hemoglobin Alc and hypertension. Type 2 diabetes is often assumed to be asymptomatic. However, an increase in urination
lethargy has been reported in a majority of patients. There are pharmacological and nonpharmacological treatments to manage type 2 diabetes.
Pharmacological treatments can vary depending on the severity of the type 2 diabetes, nonpharmacological approaches recommended are diet and
exercise. The pathophysiology of type 2 diabetes occurs mainly in the brain, neurons and other non–insulin dependent tissues, in which 75% of the total
body glucose disposal is

Cardiovascular Disease ( Cvd ) Is A Global Pandemic
Cardiovascular disease (CVD) is a global pandemic. Whereas CVD was once a relatively minor disease, it has matured into the killer responsible for
30% of global deaths each year1. Although its prevalence is high and its manifestation assumes the forms of numerous diseases, many of those who
suffer from CVD share a commonality: high blood pressure2. By increasing the chances of stroke, congestive heart disease, and heart failure,
hypertension is a major risk factor of CVD. As of the year 2000, one billion of the world's population had hypertension, with the number expected to
rise to 1.56 billion by 20251. While countries still undergoing economic development have the highest prevalence of hypertension, the Western world
suffers from it as ... Show more content on Helpwriting.net ...
Salt Sensitivity Hypertension exists in various forms such as secondary, resistant, and pseudo–resistant. Whereas the pathogeneses of pseudo–resistant
and secondary hypertension are known and treatable, the causes of resistant hypertension remain elusive, making it the most troublesome of the three5.
Resistant (also known as idiopathic or essential) hypertension is a blood pressure exceeding 140/90 mm Hg that refuses to drop despite being treated
with three or more drugs (one of which is a diuretic) at maximum doses. Obesity, increasing age, and kidney disease are suspected of contributing to
resistant hypertension, but the exact mechanisms remain unclear6. Peaking the curiosity of researchers is that the most common factor in those with
resistant hypertension is excessive salt consumption5, leading to studies of how salt intake affects blood pressure. When experimenting on single
individuals, researchers found a correlation between salt intake and blood pressure. But when they tested this correlation in large populations, it
diminished7. To account for this discrepancy the theory of salt sensitivity was developed. For some individuals an increase in salt intake raises their
blood pressure, but for others the excess salt exerts marginal effects on pressure. The former were dubbed salt–sensitive (SS) and the latter
salt–resistant (SR)8. The Pressure–Natriuresis Curve To understand salt sensitivity one must first understand sodium balance in an

Cardiac Hypertrophy Research Paper
Cardiac Hypertrophy
This paper will discuss Cardiac Hypertrophy. There are two types that will be discussed as far as the physiological and pathological hypertrophy,
which was taken from three articles discussed in class and other scholarly articles.
The heart is divided into four columns: Left and Right Arteries and the Left and Right Ventricles. The walls of the four chambers are made up of
the thick muscle (McMullen et al., 2007). There are two types of growth in the human body. Hypertrophy refers to the increase of the size of cells
that make the whole area larger. This is how cells grow through hypertrophic method. Secondly, Hyperplasia is the division of cells. This is when there
are low levels of cells being produced. The heart has ... Show more content on Helpwriting.net ...
Molecular distinction between physiological and Pathological caridiac Hypertrophy: experimental findings and Therapuetic strategies . Volumer 128
issue 1, pg 191–227. october 2010.
Ichihara, S., Senbonmatsu, T., Price, E., et al. Angiotensin II type 2 receptor is essential for left ventricular hypertrophy and cardiac fibrosis in chronic
angiotensin II–induced hypertension. Circulation. 2001; 104: 346–351.
McMullen, J.R., Jennings,G.L. Differences between Pathological and Physiological Cardiac Hypertrophy: novel therapeutic strategies to treat heart
failure. 2007, April;

Most Common Treatments For Heart Failure
One of the most common treatments for heart failure is ACE inhibitors. ACE inhibitors have shown to slow down the course of heart failure and
decrease cardiovascular mortality (1). Overall, they work by suppressing the activity of angiotensin II. ACE inhibitors prevent the conversion of
angiotensin I to angiotensin II by competitively inhibiting the activity of the angiotensin converting enzyme. Since angiotensin II is a vasoconstrictor,
the lack of the protein allows blood vessels to remain dilated which decreases blood pressure. In addition, the lack of angiotensin II decreases
aldosterone release which further lowers the blood pressure and puts less strain on the heart. Angiotensin II has been shown to be involved in the
myocardial ... Show more content on Helpwriting.net ...
In addition, the mass of viable myocardium in the treated participants increased relative to the control group. These results indicate that treatment with
CDCs was somehow able to shrink the scar tissue and stimulate the growth of myocardial tissue. However, the partial regeneration at the affected
regions did not necessarily translate to improved heart function. The ejection fraction of the treatment group only increased from 39% to 41%. It was
theorized that the introduced CDCs activated endogenous regenerative pathways through physical contact and the release of paracrine factors.
Proposed Therapy:
It was originally believed that cardiac stem cells can be transplanted into the infarcted region of a failing heart so that they can proliferate and
differentiate into cardiomyocytes to improve the heart's ability to pump blood. While transplanted cardiac stem cells were shown improve cardiac
function in animal trials and clinical trials, it was later discovered that they did so with the release of paracrine factors, not through differentiation. As
a result, interest in the use of paracrine factors to promote endogenous cardiac regeneration has increased. A proposed therapy to take advantage of the
regenerative properties of paracrine factors is to upregulate, through genetic engineering, a cardiac stem cell's release of factors SCF and IGF–1.
Both IGF–1 and SCF have shown to be potentially useful for heart

Diabetic Microvascular : Leading Cause Blindness
Diabetic microvascular complications are the leading cause of blindness, end–stage renal diseases, and other neuropathies due to hypoxia and ischemia
in the retina, the kidney, and nerves. Thickening of the capillary basement membrane result in decreased tissue perfusion. Many people with type 2
diabetes present with microvascular complications because of the long duration of asymptomatic hyperglycemia that usually precedes diagnosis
(Mccaine and Huther).
Diabetic Retinopathy
Diabetic retinopathy is the leading cause of blindness globally and in the U.S. adults younger than age 60. It is more common in individual with type
2 diabetes compared to those with type 1 due to long–standing hyperglycemia before diagnosis. Most people with diabetes eventually develops some
degree of retinopathy and they are more likely to develop cataracts and glaucoma. The prevalence and severity of retinopathy are strongly related to
individual's age, the duration of diabetes, and the extent of glycemic control. Three stages of the retinopathy leads to vision loss; stage I –
non–proliferative is characterized by thickening of the retinal capillary basement membrane and increased retinal capillary permeability, vein dilation,
micro–aneurysm formation, and hemorrhages. Stage II – pre–proliferative there is progression of retinal ischemia with areas of inadequate perfusion
that result in infarcts. Stage III – proliferative involves neovascularization (angiogenesis) and fibrous tissue formation within

Hypertension : The Most Common Chronic Disease ( Barranger )
Hypertension is one of the most common chronic disease (Barranger, 2013). Many people are unaware of the fact that they have hypertension because
they do not have any symptoms associated with this chronic disease. Hypertension can be a major risk factor for many other chronic diseases such as
heart disease, stroke, congestive heart failure, and kidney disease. Hypertension is strongly associated with obesity and diabetes. Hypertension caused
morbidity and mortality are the highest, occur early and more severe among African American's (Barranger, 2013).
Essential hypertension is the most common type of hypertension (Barranger, 2013). Other types of hypertension include primary, idiopathic
hypertension and secondary hypertension (when other causes can be identified) (Barranger, 2013).
The pathophysiology of hypertension involves nervous system and/or renal system (Barranger, 2013). Centrally located beta receptors and alpha–2
receptors have effects on the production of norepinephrine. The production of norepinephrine is stimulated and inhibited by these receptors. When
norepinephrine production is inhibited, vasodilation effects occur, therefore blood pressure (BP) is reduced. Beta 1 receptor blockers and beta 2
receptor stimulators of the arteries and veins will decrease blood pressure by decreasing cardiac output, peripheral resistance, and causation of
vasodilation. Baroreceptors can auto regulate blood pressure in the circulatory system by sending impulse to the brain

Analysis Of Hypertension : The Silent Killer Of The Heart
Sophia Medina
Dec 3, 2017
Hypertension: The Silent Killer of the Heart
"You are what you eat" is a notable phrase, commonly used throughout the United States. This famous saying is known to have emerged from the
French statement, "Dis–moi ce que tu manges, je te dirai ce que tu es." It is translated in English to say, "tell me what you eat, and I will tell you what
you are." This phrase was published in 1825 in the book, The Physiology of Taste or Meditations on Transcendental Gastronomy, written by Jean
Anthelme Brillat–Savarin, a French judge, politician, and author.
The underlying concept of the phrase exemplifies that one's health and well–being are interrelated with what one consumes. For example, just as excess
sugar consumption can lead to weight gain, the amount of salt consumption is known to have a direct correlation to the level of blood pressure in
humans.
Blood pressure is an important vital sign to keep track of. In 2014, high blood pressure was the primary or contributing cause of death in the United
States (Centers for Disease Control and Prevention). Therefore, monitoring blood pressure is imperative. If not managed, there is a greater risk of
developing dangerously high blood pressure levels leading to chronic cardiovascular diseases.
Throughout this paper, I will state the cardiovascular system's role in the body and define the elements that compose blood pressure. As well as
emphasize the risk factors, pathophysiology, and management of hypertension.

Reference Guide for Pharmacy Technician Exam Essay
Reference Guide for Pharmacy Technician Exam
Krisman
REFERENCE GUIDE
FOR PHARMACY
TECHNICIAN EXAM
EDITION 2014–2015
(Covers an updated 2013–PTCB Blue Print)
MANAN SHROFF
www.pharmacyexam.com
1
Reference Guide for Pharmacy Technician Exam
Krisman
This reference guide is not intended as a substitute for the advice of a physician. Students or readers must consult their physicians about any existing
problem. Do not use any information in this reference guide for any kind of self treatment. Do not administer any dose of mentioned drugs in this
reference guide without consulting your physician. This is only a review guide for preparation for the pharmacy technician board exam. The author of
this reference guide ... Show more content on Helpwriting.net ...
Thrombocytopenia: A low platelets count inblood.
Ventricular arrhythmia: Irregular movements of left ventricles of the heart.
2–ANTIARRHYTHMIC AGENTS

M/A: This class of agents is indicated for the treatment of an irregular heart rhythm.
Brand
Generic
Cordarone
Amiodarone
Norpace
Disopyramide
dry

Advantages And Disadvantages Of Valsartan
DEVELOPMENT & EVALUATION OF FAST DISINTEGRATING FILMS AND TABLETS OF VALSARTAN G.Sandhyarani 1,M.Madhuri 2 1,2
vaageswari college of pharmacy,Karimnager Corresponding Author:Sandhyaguggilla9@gmail.com Abstract Orodispersible dosage forms are used for
accurate dosing, enhanced bioavailability, rapid action, patient compliance, easy of administration, enhanced palatability. Valsartan is a specific and
selective type–1 angiotensin II receptor antagonist which blocks the blood pressure increasing effects angiotensin II via the
renin–angiotensin–aldosterone system. Valsaratan orodispersible films are prepared using all polymers HPMC E3,HPMC E15,HPMC 5cps,HPMC
15cps,HPMC 50cps, HPMC 50cps+CP in 39.68 mg., 59.52 mg quantity... Show more content on Helpwriting.net ...
The drug release was found to be fast in ODFs than ODTs. REFERENCES C.P.Jain and P.S. Naruka. Formulation and Evaluation of Fast dissolving
Tablets of Valsartan. International Journal of pharmaceutical Sciences, Vol 1. Issue 1. July
–Sept 2009 Choudhary DR, patel VA , kundawala AJ,
Formulation and evaluation of quick dissolving Film of levocetirizine dihydrochloride , Int J Pharma Tech ,2011;3 (1) :1740–1749 Saini S , NandaA .,
Dhari J., Formulation, development & evaluation of oral fast dissolving anti–allergic film of levocetrizine dihydrochloride , J. Pharm. Sci. & Res.,
2011;3(7):1322–1325 Raju S., Reddy P., Kumar V., flash release oral films of metoclopramide hydrochloride for pediatric use: formulation and in
–vitro
evaluation, j. Chem. Pharm. Res., 2011;3(4):636–646 Patil SB.,Shahi SR., Formulation and evaluation of quick dispersible tablet of Olanzapine , Int J
Pharma . Res.Dev.,2009; 7(!),30–34 Mishra R and Amin A., Formulation and Characterization of Rapidly Dissolving Films of Cetirizine hydrochloride
using Pullulan as a Film Forming Agent ,Ind J Pharm Edu Res, 2011; 45(1)

Ventricular Remodelling
Heart failure is a condition where the heart is unable to pump insufficient amount of blood to supply the rest of the body. This is a consequence of
ventricular remodelling. Ventricular remodelling is a term that refers to alterations in structure, shape and function of the left ventricle. (1) The
activation of neuro–hormonal systems such as RAAS and the sympathetic nervous system are predominantly linked to the pathophysiology of heart
failure. Therefore, interrupting this system is vital to delaying the progression of heart failure. (2)
Valsartan is an Angiotensin II receptor antagonist selective for the type I (AT I) angiotensin receptor which mediates the release of aldosterone. A
receptor antagonist, such as valsartan, has an affinity ... Show more content on Helpwriting.net ...
However, this endopeptidase also breaks down the protein beta amyloid in the human brain and is thought to be the rate limiting step in amyloid beta
degradation. (14) A build up and abnormal misfolding in neural tissue of beta amyloid plaques is linked to the origin of Alzheimer's disease.
Therefore, by using sacubitril it inhibits the neprilysin enzyme by breaking down the beta amyloid plaques in the brain. However, the vascular benefits
of the drug may at the same time protect against Alzhiemer's disease. For example, as the drug causes an increase in blood flow this could speed up the
clearance of the beta build up in the brain.

Nurse
Medication Sheet Medication/Dose/RouteClassificationGeneric/Trade Name| Action| ContraindicationAdverse Effects| Nursing Considerations|
Acetaminophen/500mg/ By MouthAntipyretic& Analgesic (nonopioid)Acetaminophen/TylenolCarvedilol/6.25mg/By MouthAlpha– and
beta–adrenergic blocker & AntihypertensiveCarvedilol/CoregDocusate Sodium/100mg/By MouthLaxative stool softenersDocusate Sodium
/ColaceFurosemide/40mg/By MouthLoop diureticsFurosemide/Lasix| Reduces fever by acting directly on the hypothalamic heat–regulating center to
cause vasodilation and sweating, which helps dissipate heat.Carvedilol causes vasodilation by blocking the activity of О±–blockers, mainly at alpha–1
receptors. It exerts antihypertensive effect partly by... Show more content on Helpwriting.net ...
WD.com recommends enquiry into: diet and lifestyle; duration of constipation and whether it is acute or chronic; all medications taken, whether
prescribed over the counter or recreational; associated symptoms such as bleeding from the rectum, abdominal pain, vomiting. Implementation: Oral
preparations of Colace should be administered on an empty stomach at least one hour apart from other medications, meals, milk and antacids. It may be
given in juice to prevent possible throat irritation. Six to eight ounces or 180–240 ml of water should be taken with oral preparations. When
administering rectal preparations, beware of forcing past impacted feces. Discontinue the medication at the first sign of nausea and vomiting,
abdominal cramps or rectal bleeding.http://preventconstipation.methodsofprevention.com/colace–nursing–considerations/Assessment: Assess fluid
status. Monitor daily weight, intake and output ratios, amount and location of edema, lung sounds, skin turgor, and mucous membranes. Notify health
care professional if thirst, dry mouth, lethargy, weakness, hypotension, or oliguria occurs. Monitor BP and pulse before and during administration.
Monitor frequency of prescription refills to determine compliance in patients

Symptoms And Treatment Of Hypertension Essay
3.According to the B.P value, what stage of hypertension is M.K. experiencing? Explain the rationale for her current medications for her hypertension.
Also, discuss the impact of this disease on the U.S population. According to the blood pressure in the assessment, M.K. has stage one hypertension. It
was noted that she is currently being prescribed Lasix and Lotensin to help with her high blood pressure. Lotensin, also known as Benazepril, is an
ACE–inhibitor, or angiotensin–coverting enzyme inhibitor. These types of drugs play an important role in the RAAS (which stands for
renin–angiotensin–aldosterone system). Arterial blood pressure is regulated and accomplished through neural, hormonal, and renal interaction and is in
tune with the homeostatic fluid volume of one's body. The balance of sodium and water is performed by the kidneys and the
renin–angiotensin–aldosterone system is the main regulator of fluid volume in the body. An increase of extracellular fluid increases vascular
resistance, which in turn leads to increased arterial blood pressure. The kidneys will then sense this pressure change and in order to compensate, will
promote sodium and water loss through micturition. Sodium intake is directly proportional to arterial blood pressure and since the kidneys cannot get
rid of sodium as fast as water, higher levels are expected. As sodium increases serum osmolality triggering the hypothalamus to act as the regulator by
signaling the posterior pituitary gland to

Potential Health Risks from Inappropriate Prescription of...
Learning Goals
1) Locate where in the renin–angiotensin–aldosterone pathway ACE inhibitors act
2) Identify commonly prescribed antihypertensive medication by primary care physicians
3) List 3 possible side effects from inappropriate ACE inhibitor prescription
4) Suggest possible regulations of ACE inhibitor use for primary care physicians and alternative treatment plans for patients
Introduction
Cardiac related diseases account for over 56 million annual deaths worldwide.1 Cardiovascular disease (CVD) is the leading cause of death in
economically developed countries and is increasing in occurrence in developing nations.1 The prevalence of CVD increases with age.1 The mean
level of blood pressure, used to diagnose CVD, is higher in ... Show more content on Helpwriting.net ...
She has been smoking a pack of cigarettes per day for the past 20 years. She has admitted to occasional alcohol use. She is allergic to the commonly
prescribed antibiotic penicillin.
Biochemical Mechanisms of ACE Inhibitors
The renin–angiotensin–aldosterone system (RAAS) is a group of hormones that are produced sequentially in order to regulate salt–water homeostasis as
well as blood pressure.5 The first enzyme, renin, is produced by the juxtaglomerular cells of the kidney when blood volume is low and is released into
the bloodstream.3,5,6 Renin then catalyzes the conversion of angiotensinogen to angiotensin I.3,5,6 Angiotensin–converting enzyme (ACE), which is
produced in the lungs, subsequently converts angiotensin I to angiotensin II, a more active enzyme.3,5,6 Angiotensin II has several functions. The
hormone's primary mechanism for increasing blood pressure is through the stimulation of blood vessel constriction. Furthermore, angiotensin II
increases the contractility of the heart via sympathetic activation. It also stimulates anti–diuretic hormone (ADH) release, which increases water
reabsorption at the collecting ducts, resulting

Hypertension : Hypertension And Essential Hypertension Essay
Hypertension is widely considered to be one of the most important risk factors of cardiovascular diseases (angina, arrhythmia, etc.). It is the second
leading disease that causes mortality in the world. Hypertension is the condition when there is an increase in the force of blood on the walls of vessels.
It can also be defined as an arterial blood pressure that is raised above 140/90 mm Hg (systolic/ diastolic BP). Hypertension can be classified into
Secondary hypertension and Essential hypertension. When specific cause is evident but heredity, and various physiological parameters play a role in
increasing blood pressure is known as Essential Hypertension. Secondary Hypertension is one where the cause is known. According to WHO
guidelines between 2006 and 2015, deaths due to cardiovascular diseases are expected to increase by 17% while the deaths from infectious diseases,
nutritional deficiencies, maternal and prenatal conditions are projected to decline by 3%. The main causes of hypertension includes the age ,hereditary,
gender, extra weight, alcohol consumption, stress life, lazy life etc.
Basically, arterial blood pressure (BP) is directly proportional to the product of blood flow (cardiac output, CO) and the resistance to passage of blood
through pre–capillary arterioles (peripheral vascular resistance, PVR) Hypertension can be caused by either an increase in Cardiac Output (CO) or by
an increase in Peripheral Resistance (PR) BP = CO X PVR
Renin Angiotensin

The Effect Of Salt Intake On Hypertensive Vs. Individuals
Effect of Salt intake on Hypertensive vs. Normotensive Individuals
Syed Muhammad Raza Zaidi, B.Sc., MD Candidate
Medical University of Americas
Syed Zaidi
42B–5305 Glen Erin Drive,
Mississauga, ON
L5M 5N7
Phone #: (647) 767–6347
Email: syedxeidi@gmail.com
I would like to extend special thanks to all authors that have contributed to the intellectual property that was central to the compilation of this work.
Mentor: Dr. Vivek Joshi
Word Count: 4388
Hypothesis:
Decreasing salt intake by hypertensive patients can significantly decrease the MAP (Mean Arterial Pressure) and bring it in the normal range, thus, this
strategy can be used to effectively manage hypertension in mild to moderate hypertensive patients.
Table of Contents:
Ultramini Abstract3
Abstract3

Introduction4
Methods5
Results6
Discussion12
Conclusion17
Appendix18
References22
Ultramini Abstract
This report is a compilation and analysis of the current and latest literature to verify the harms of sodium intake and to develop ways to mitigate the
harms and improve health in societies and the people most at risk. The results indicate that changing diets and reducing sodium intake can effectively
help manage hypertension and related complications.
Abstract
Hypertension is one of the leading causes of mortality in the developed world. It is integral to explore the different causes of hypertension, especially
high sodium diets, and its management to decrease the morbidity

Different Pathways Of Allorecognation : Direct, Indirect,...
There are three pathways of allorecognation: direct, indirect, and linked pathways. The difference of direct and indirect pathways is the work of
dendritic cells in presenting the donor peptides as foreign antigens. In direct pathway, the dendritic cells migrate directly from the graft into the
recipient's lymph nodes and present the antigen to their own MHC to T cell receptor (TCR). This will excite an anti–donor T–cell allorecognition
response and lead to rejection. Both CD4+ and CD8+ are capable for this. Conversely, in indirect pathway, the dendritic cells migrate to the graft,
take and process some proteins from the recipient cells and present it on MCH to T cells in lymph nodes. While, linked allorecognation is by using
direct transfer of cell membrane from donor dendritic cells to recipient dendritic cells.3,4 (Figure 2) There are six MHC class I isotypes: HLA–A,
HLA–B, HLA–C, HLA–E, HLA–F, and HLA–G while for MHC class II : HLA–DM, HLA–DO, HLA–DP, HLA–DQ, and HLA–DR. As the fact that
every single person has different type of HLA and may be provided as a foreign antigen in other individual, HLA take significant role on the rejection
response in organ transplantation.1,2 Chronic Rejection in Organ Transplantation Chronic rejection is characterized as a slow process of a tissue
replacement in allograft into fibrous scar tissue as fibroproliferative changes by some immune (antigen–dependet) and non immune factors
(antigen–independent).4 Chronic Rejection may takes

Sleep Disturbance And Day Time Sleepiness
which his characterized by snoring, sleep disturbance and day time sleepiness. There is a close relation between OSA and hypertension; as many as
one–third of hypertensive patients and above 80% of those with resistant hypertension have OSA.
Alcohol– Higher intake of alcohol increases the blood pressure. Reducing alcohol leads to fall in the systolic blood pressure.
Stress– Psychological or environmental stress play a part in the causes of hypertension. Direct effects of situations such as poverty, unemployment and
poor education (stressors) are involved, as are other aspects of lifestyle that are linked to hypertension.
Exercise– Physical activity increases blood pressure, but people who exercise regularly have lower blood pressures. Such people, however, also may
have a healthier diet and more sensible drinking and smoking habits.
Other dietary factors– Vegetarians generally have lower BP than non–vegetarians. Reducing a meat rich diet with vegetable products reduces blood
pressure. Caffeine and caffeinated drinks also increases blood pressure and must be avoided.
THE VARIOUS BODY MECHANISMS THAT CAUSES AND INFLUENCES HYPERTENSION
The various mechanisms that cause and influences hypertension are actually built into us for good reasons: we need them to keep our blood pressure
from falling too low. But when they go somewhat awry, they cause high blood pressure. And when that happens, we need treatment for hypertension,
ironically aimed at the same mechanisms.
1. How

Hypertension Is Characterized By Chronic Elevated Blood...
Background
Hypertension is characterized by chronic elevated blood pressure1. It can be a predisposing factor or secondary to heart failure. In the US, there are
75 million individuals who have hypertension with two thirds of individuals 65 years or older diagnosed. Various factors can contribute to the
development of hypertension including renal disease, thyroid disease, dysregulation of hormones, and alcohol consumption. The disease also highly
correlates with age as even individuals 55 years old with normal blood pressure have a 90% lifetime risk of developing hypertension with age. Left
untreated, hypertension can result in retinopathy, cardiomyopathy, and stroke with the most common cause of death being coronary artery disease.
The diagnoses of hypertension is primarily done by the monitoring of blood pressure with multiple readings of systolic pressure greater than 140 mmHg
and diastolic pressure greater than 90 mmHg indicating stage one hypertension1,2. The evaluation of the eyes, heart, thyroid, and renal system are also
important in understanding the cause and extent of hypertension. Initial treatment involves lifestyle and diet modifications such as exercise, smoking,
cessation, and limited sodium intake. Patients unresponsive to lifestyle and diet modification or have a blood pressure greater than 160/100 mmHg are
recommended by the American Heart Association to begin drug therapy. Current JNC–8 guidelines dictate the goal of treatment to reduce blood pressure

Renin Angiotensin Aldosterone System Analysis
Renin Angiotensin Aldosterone System (RAAS) is the system that regulates blood pressure in the body. When the body detects low blood pressure
(low fluid/low salts), the liver releases angiotensinogen (Bayer pharma, 2015). The release of the angiotensinogen is the beginning of the signal
transduction pathway (Bayer pharma, 2015). The angiotensinogen and renin react together to form angiotensin I, then angiotensin–converting enzyme
(ACE) converts angiotensin I into angiotensin II (Bayer pharma, 2015). Angiotensin causes vasoconstriction in the blood vessels, secretes the
water–retaining hormone vasopressin (AVP) from the pituitary gland, and also releases adrenaline, noradrenaline, and aldosterone from the adrenal
gland (Bayer pharma, 2015). Overall blood pressure is most prominently regulated by the peptide angiotensin II. The angiotensin II controls
vasoconstriction through the regulation of water and salt balance (Lopez 2003). The RAAS is an essential pathway for the body to regulate blood
pressure in the body, but this pathway ... Show more content on Helpwriting.net ...
ATRAP is found in many organ systems of the body but the highest concentration of ATRAP is found in the kidneys (Giani 2013). With the advances
of gene targeting technology, the physiological role of ATRAP has been better defined (Giani 2013). For example in the experiment Angiotensin II type
1 receptor–associated protein: a novel modulator of angiotensin II actions in the nephron they eliminated ATRAP from the system it showed an
elevation in blood pressure by about 8mm/Hg in mice (Giani 2013). In the experiment Giani found that mice with ATRAP knockout had elevated
plasma and blood volume, which means the absence of ATRAP caused increased sodium and water retention by the kidneys (Giani 2013). Through the
experiment Giani concluded that ATRAP was a blood pressure modulator based on ATRAP's negative effects on proximal tubular ATR function (Giani

Atrap, And Angiotensin Receptor Associated Protein
Introduction:
ATRAP, or Angiotensin Receptor Associated protein, is a cytoplasmic protein that is found to interact with the carboxyl
–terminal domain of
Angiotensin type 1 receptors (AT1) (Cui et al., 2000). ATRAP was discovered to have three hydrophobic domains located at the amino
–terminal end
and one long hydrophilic tail found at the carboxyl–terminal end (Lopez–Ilasaca et al., 2003). This 18–kDA protein is highly specific in it's binding and
is predicted to have three transmembrane domains along with a cytoplasmic tail. ATRAP fails to bind to various other receptors, which exclude AT1
(Castrop, 2015). In yeast, the orientation of the protein was seen to have the amino end outside the cell. In addition, mutant proteins, which did not
have the carboxyl end, were unable to bind to the AT1 receptors (Lopez–Ilasaca et al., 2003).
In order to understand the role of ATRAP in humans, it is imperative to understand the role of the AT1 receptor itself. AT1 receptors are crucial
elements of the renin–angiotensin system. They act as mediators for almost all physiological roles of angiotensin II (AngII). Inhibiting the binding of
angiotensin II to AT1 receptors can effectively lower blood pressure of patients who are found to have hypertension. This observation demonstrates that
AT1 receptors, more specifically those found in the kidneys, are important factors in the cause of hypertension in humans (Chen & Coffman, 2015).
After understanding regulation model, the function of

ACE Inhibitors
ACE, which stands for Angiotensin Converting Enzyme, is an enzyme that is classified as a kinase II compound (1). ACE inhibitors are
antihypertensive agents that work to slow down the activity of the ACE enzyme. ACE inhibitor medications are used to help patients with high blood
pressure as well as those who are high risk of getting coronary artery disease, post heart attack, kidney disease and diabetes (2). ACE inhibitors are
membrane–bound dipeptidyl carboxypeptidases that regulate the renin–angiotensin system (RAS) (3). There are two forms of ACE in humans, somatic
ACE and testis ACE, which regulate blood pressure (3). ACE Inhibitors are found in endothelial, epithelial or neuroepithelial cells as well as the brain
(1). The physiological ... Show more content on Helpwriting.net ...
While captopril is the only ACE inhibitor that contains a sulfhydryl group, fosinopril contains a phosphate group. The remaining ACE inhibitors are
dicarboxyl–containing compounds as seen in Figure 2. Captopril has duration of 6 to 12 hours, while most other ACE inhibitors last for approximately
24 hours (2). The oral bioavailability of captopril is 75%; the elimination half–life is less than 2 hours. Approximately 50% of the dose of captopril is
excreted in the urine without any changes to the structure; the remaining 50% is converted into a disulfide dimer. For enalapril, the oral bioavailability
is 60% and the elimination half–life is 11 hours. The metabolism and elimination of this form of the drug is done by hydrolyzing the compound to
form a more portent compound, enalaprilat. After, no further metabolism is required and both the enalapril and enalprilat go through renal excretion
(2). Drugs that contain carboxyl groups, like enalapril, are esterified with an alcohol to make them more lipophilic, increasing absorption. After the
drug is absorbed, it is hydrolyzed by carboyxlesterase and enaliprilat is released. While enalapril is an inactive prodrug, enalprilat is the active ACE
inhibitor metabolite. Lastly, fosinopril has an oral bioavailability of 36% and a half–life of 12 hours. Fosinopril is hydrolyzed to form fosinoprilat and
is eventually excreted in the urine and bile (2). A comparison of these values can be seen in Table

Ang 2 Research Paper
Angiotensin II (Ang II) is one of the mechanisms that elevates the blood pressure, and is most well known for as being a systemic vasoconstrictor.
When Ang II binds to the receptors that are throughout the body, it affects on constricting the blood vessels, which therefore increases the blood
pressure. It also has an affect on the kidneys, which increases the sodium retention and hence, altering the process of filtering blood. This then increase
the water reabsorption in the kidney, which causes to increase blood volume and also blood pressure (1). Recently, it has been suggested that the role
of Ang II may be linked to the physiological and pathological effects to the homeostasis of ER stress of Type 2 Diabetes.
The endoplasmic reticulum (ER) stress has emerged as one of the major pathophysiological mechanism of various diseases. It is a multifunctional
cellular organelle and it is responsible for protein synthesis, folding, trafficking, processing transmembrane proteins and is also known as a primary
sensor for cellular stress (2). In order for the ER proteins to be folded properly, there must be a balance between the ER proteins and the amount of
folding capacity for it to process. However, the ER homeostasis may be disrupted which could cause the accumulation of unfolded and misfolded ...
Show more content on Helpwriting.net ...
It is a common form of diabetes and affects about 85 to 90 per cent of all people with diabetes (5). The cells in the body of Type 2 Diabetes patients
do not respond to insulin properly, which is known to be insulin resistance or deficiency. Therefore, glucose builds up in the blood rather then getting
into the cells for energy (6). Recent studies suggest that different forms of emotional stress could lead to Type 2 Diabetes. Other studies also suggest
that depression, anxiety and anger may be associated with the development of Type 2 Diabetes

Introduction And Learning Objectives Of Heart Failure
Introduction and Learning Objectives
Heart failure is a debilitating condition, affecting around 1–2% of the UK population (Sutherland, 2010). Its prevalence is rising due to an increase in
its risk factors, most notably an increased population life expectancy (Patient.co.uk, 2014). In the scenario Mr Williams is an obese 65–year–old man,
exhibiting numerous symptoms indicative of congestive heart failure. In this PBL write–up, I aim to explore the issues raised, whilst relating them to
the pathophysiology of heart failure.
Learning Objectives
Whilst discussing the scenario, our group came up with the following objectives:
1.Define any unknown terms
2.What is heart failure?
3.Explain the signs and symptoms presented by Mr Williams
4.Diagnosis of heart failure
5.Treatment of heart failure
Unknown Terms
We identified "pulsus alternans" as an unknown term from the scenario.
Pulsus Alternans is characterised by alternate strong and weak beats during a regular sinus rhythm (Weber, 2003). The systolic pressure can vary up to
50mmHg between beats (Kumar and Clark, 2009).
What is heart failure?
Heart failure is a result of any structural or functional cardiac disorder, leading to an impaired ability of the heart to pump a sufficient circulation to
metabolising tissues (Sutherland, 2010). It can also be called "congestive heart failure", as fluid retention is a common symptom. The main causes of
heart failure are ischaemic heart disease, cardiomyopathy and hypertension

Pathophysiologic Model
Cardiovascular function results from the interplay of the heart, systemic vasculature, blood volume, and tissues in their functions as pump, transporting
pathways, and oxygen carrying and consuming end–organs, and problems with structure or function of the filling and ejection mechanisms of the heart
will lead to failing oxygen delivery and compensatory attempts, a complex disease condition known as heart failure (Porth, 2015). Dysfunction may
involve initially primarily one ventricle only, though over time both sides may become affected. In left ventricular failure decreased cardiac output and
outflow into the periphery leads to pulmonary congestion, evidenced by pulmonary edema and impaired gas exchange (Porth, 2015). As a result,...
Show more content on Helpwriting.net ...
Baroreceptors activate the sympathetic nervous system, with an increase in heart rate and blood pressure and vasoconstriction, causing beta receptor
downregulation, and further increased adrenergic tone with pathological activation of the renin–angiotensin–aldosterone–system (Johnson, 2014).
Angiotensin II releases catecholamine and stimulates renin release, which raises tone and pressure on the heart, and leads to aldosterone secretion, also
increasing the pressure load on the heart; water and sodium retention through the presence of vasopressin and aldosterone add to preload (Johnson,
2014). This model is used to explain the compensatory mechanisms employed to maintain cardiac reserve, the ability of the heart to respond to
increased needs; additional neurohormonal changes involve natriuretic peptides, atrial natriuretic peptide, brain natriuretic peptide and endothelin 1
(Johnson, 2014; Porth,

The Cardiovascular System: Angiotensin
Angiotensin II is an octapeptide which is associated with the cardiovascular system. It maintains blood pressure by vasoconstriction and stimulation of
aldosterone secretion. Angiotensin II is synthesized through the renin–angiotensin system (RAS) which is known to be involved in systemic blood
pressure control, including the regulation of cerebral blood flow (Mogi, Iwanami, & Horiuchi, 2012). Renin, a product of the juxtaglomerular cells of
the kidney, is released into the circulation where it cleaves the angiotensinogen to form angiotensin I. Angiotensin I is cleaved by
angiotensin–converting enzyme (ACE) to form the angiotensin II. Apart from the production of angiotensin II in plasma and peripheral organs such as
kidney, adrenal gland, ... Show more content on Helpwriting.net ...
Both receptors are differentiated by their selective affinity for different non–peptide ligand although they have the similar binding for angiotensin II
(De Gasparo, Catt, Inagami, Wright, & Unger, 2000). Both receptors belong to the seven–transmembrane domain, G–protein coupled receptor family
(Saavedra, 2005). However, AT2 receptor shares only 32
–34% amino acid identity with the AT1 receptor. AT1 receptor was found in the areas related
to neuroendocrine control and autonomic regulation of cardiovascular function and the limbic system (Tsutsumi & Saavedra, 1991). The
physiological actions of angiotensin II in the brain, such as regulation of blood pressure, fluid balance, and hormone secretion, are mediated by the
AT1 receptor. Additionally, systemic angiotensin II affects the brain functions through AT1 receptors located in the circumventricular organs which
are devoid of BBB and derived angiotensin II may act at many sites in the central nervous system located behind the BBB (Unger & Scholkens,
2004). On the other hand, AT2 receptor acts a role in brain organogenesis and in the function of sensory and motor systems (Tsutsumi & Saavedra,
1991). However, the physiological functions of the AT2 receptor are still uncertain (De Gasparo & Siragy, 1999; Saavedra, 2005). Thus, the role of
brain angiotensin II appears to be multiple and complex

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