antihypertensive_agent

Faculty of nursing
Antihypertensive agent
Presented by
Omar AL_qaisi and Ahmad Al_masry

Content outline
 Overview
 Classification of antihypertensive agent
 Mechanism of action of antihypertensive agent
 Side effect of antihypertensive agent
 Toxicity of antihypertensive agent
 RESEARCH

Overview
• Hypertension isdefinedaseitherasustainedsystolicblood pressure(SBP)ofgreaterthan
140mmHg or asustaineddiastolicbloodpressure(DBP) ofgreaterthan90mmof
Hg.(Barbé, F., Durán-Cantolla, J., Capote, F., de la Peña, M., Chiner, E., Masa, J. F., ... & Montserrat, J. M. (2010))
• Antihypertensive areaclassofdrugsthatareusedto treathypertension
highbloodpressure).(Joshi, V. D., Dahake, A. P., & Suthar, A. P. (2010).)
• Evidencesuggeststhatreductionofthebloodpressureby5 mmHgcandecreasetheriskof
strokeby34%,ofischemicheart. (Law, M., Wald, N., & Morris, J. (2003).
 Diseaseby21%,andreducethelikelihoodofdementia,heartfailure,andmortality
fromcardiovasculardisease.
(
Appelros, P., Nydevik, I., Seiger, A., & Terént, A. (2002). )

Classification of antihypertensive
agent
1. Diuretics
2. Beta adrenergic drug
3. Calcium channel blocker
4. Angiotensin receptor blocker
5. Angiotensin converting enzyme inhibitor
6. Direct arterial vasodilator
7. Sympatholytic and adrenergic blocker

agent
 Diuretics:
 Diuretics are a class of drugs that increase the production of
urine by the kidneys, leading to a reduction in the amount of
fluid and sodium in the body.
 There are several different types of diuretics, which are
classified based on their mechanism of action and chemical
structure.

agent
 The three main classes of diuretics are:
 Thiazide diuretics: These drugs act on the distal
convoluted tubule of the nephron in the kidney and
inhibit the reabsorption of sodium and chloride ions. This
results in increased excretion of sodium, chloride, and
water, and a reduction in blood volume and blood
pressure. Examples of thiazide diuretics include
hydrochlorothiazide, chlorthalidone, and indapamide.

Cont.
 Potassium-sparing diuretics: These drugs act on the
collecting ducts of the kidney and block the actions of
aldosterone, a hormone that promotes sodium and water
retention and potassium excretion. This results in
increased excretion of sodium and water, but retention of
potassium. Examples of potassium-sparing diuretics
include spironolactone, eplerenone, and amiloride.

Cont.
 Loop diuretics: These drugs act on the thick ascending
limb of the loop of Henle in the kidney and inhibit the
reabsorption of sodium, chloride, and potassium ions.
This results in increased excretion of these ions and
water, and a reduction in blood volume and blood
pressure. Examples of loop diuretics include furosemide,
bumetanide, and torsemide.

Indication of diuretics and dosage
Clinical indication and dosage:
1. Loop diuretics: used for acute edema or heart failure.
dosages vary depending on the patient's medical condition but
typically range from 20 to 80 mg per day.
1. Thiazide diuretics: used for long-term management of high blood
pressure or mild to moderate edema. Dosages vary depending on
the patient's medical condition but typically range from 12.5 to 50
mg per day

Indication of diuretics and dosage
 Potassium-sparing diuretics:
 used in combination with other diuretics to prevent
potassium loss and maintain electrolyte balance
 Dosages vary depending on the patient's medical
condition but typically range from 25 to 100 mg per day.

Side effect of diuretics
 Low sodium
 Headache
 Dizziness
 Thirst
 Muscle cramp
 Skin rashes
 Increase cholesterol
 Gout
 In rare cases , diuretics may cause serious side effect, these can
include :
 Allergic reaction
 Irregular heartbeat
 Kidney failure

toxicity diuretics and management
of Overdose
 Dehydration: The main treatment for dehydration is to replenish fluids and
electrolytes. This may involve drinking water or oral rehydration solutions,
intravenous fluids.
 Electrolyte imbalances: Electrolyte imbalances may require monitoring
and correction of the specific electrolyte levels that are affected. This may
involve oral or intravenous supplementation of the affected electrolyte.
 Hypotension: Hypotension may require supportive measures such as
raising the legs, increasing fluid intake, and administering medications to
increase blood pressure.
 Ototoxicity: Ototoxicity may be irreversible in some cases, but stopping the
use of the diuretic can prevent further damage. In some cases, medications
or other interventions may be used to manage symptoms.
 Allergic reactions: Allergic reactions may require administration of
medications such as antihistamines, corticosteroids, or epinephrine,
depending on the severity of the reaction.

 Beta adrenergic drug MOA:
 Beta-adrenergic drugs are a class of medications that bind
to beta-adrenergic receptors in the body, which are
primarily located in the heart, lungs, and blood vessels.
 There are two types of beta-adrenergic receptors, beta-1
and beta-2, which are activated by different types of
beta-adrenergic drugs.
agent

Cont.
 Beta-1 adrenergic drugs primarily affect the heart and are
used to treat conditions such as heart failure and atrial
fibrillation. Examples of beta-1 adrenergic drugs include
metoprolol, atenolol, and bisoprolol.
 The mechanism of action of beta-1 adrenergic drugs is to bind
to beta-1 receptors in the heart, which reduces heart rate and
contractility, thereby reducing the workload on the heart and
improving its efficiency.

Cont.
 Beta-2 adrenergic drugs primarily affect the lungs and are
used to treat conditions such as asthma and chronic
obstructive pulmonary disease (COPD). Examples of beta-2
adrenergic drugs include albuterol, salmeterol, and
formoterol.
 The mechanism of action of beta-2 adrenergic drugs is to bind
to beta-2 receptors in the lungs, which relaxes the smooth
muscle around the airways, making it easier to breathe.

Cont.
 In addition to their primary effects, beta-adrenergic drugs may also have secondary
effects on other parts of the body, such as the blood vessels, kidneys, and
gastrointestinal tract. These effects are mediated by the activation of other types of
adrenergic receptors or by the release of other hormones and neurotransmitters in
response to beta-adrenergic stimulation.
 Overall, the mechanism of action of beta-adrenergic drugs is to bind to beta-
adrenergic receptors in the body and produce specific effects depending on the
type of receptor and the location in the body. They are commonly used to treat
cardiovascular and respiratory conditions, among other conditions.

Indication of beta adrenergic
blocker and dosage:
1. Hypertension (high blood pressure) used as first-line therapy or as add-on
therapy for hypertension. the usual starting dose for atenolol is 50 mg once
daily, while the starting dose for metoprolol is 25-50 mg twice daily.
2. Angina (chest pain):used to treat angina by reducing the heart rate and
workload on the heart. the usual starting dose for propranolol is 40 mg
twice daily, while the starting dose for metoprolol is 50 mg twice daily.
3. Heart failure: used to treat heart failure by reducing the heart rate and
improving cardiac function usual starting dose for carvedilol is 3.125 mg
twice daily, while the starting dose for bisoprolol is 1.25 mg once daily.

Indication of beta adrenergic
blocker and dosage:
 Arrhythmias (irregular heartbeats):used to treat certain types
of arrhythmias, such as atrial fibrillation or ventricular
tachycardia. the usual starting dose for propranolol for atrial
fibrillation is 10-20 mg three to four times daily, while the
starting dose for sotalol for ventricular tachycardia is 80 mg
twice daily.

Side effect of beta adrenergic
blocker
 Fatigue or weakness
 dizziness or lightheadedness
 Headache
 Nausea or vomiting
 Insomnia or sleep disturbances
 Tremors or shakiness
 Palpitations or arrhythmias
 Hyperglycemia
 hypokalemia

toxicity beta adrenergic blocker
and management overdose
 Supportive care: Patients with beta blocker overdose may require
supportive care, such as monitoring of vital signs, oxygen therapy,
and intravenous fluids to maintain blood pressure and hydration.
 Administration of glucagon: Glucagon is a hormone that can be
used to increase the heart rate and contractility in patients with
beta blocker overdose. Glucagon is given as an intravenous infusion
or injection, and the dose varies depending on the patient's weight
and response.

toxicity beta adrenergic blocker
 Administration of high-dose insulin: High-dose insulin therapy can
be used to increase glucose uptake in the heart and other organs,
which can help to counteract the effects of beta blockers. High-dose
insulin therapy is given as an intravenous infusion, and it may be
combined with dextrose to maintain blood sugar levels.
 Administration of epinephrine: In severe cases of beta blocker
overdose, epinephrine may be used to increase the heart rate and
blood pressure. Epinephrine is given as an intravenous infusion or
injection, and the dose is titrated to the patient's response.
 Hemodialysis: Hemodialysis may be used to remove the beta
blocker from the bloodstream in patients with severe overdose.

Contraindication
 Severe bradycardia: Beta blockers can slow the heart rate, so they are generally not
recommended in patients with severe bradycardia (less than 50 beats per minute)
unless a pacemaker is in place.
 Heart block: Beta blockers can worsen heart block, a condition in which the
electrical impulses that control the heart's rhythm are disrupted. Beta blockers
should be used with caution in patients with heart block.
 Asthma and chronic obstructive pulmonary disease (COPD): Beta blockers can
cause bronchoconstriction (narrowing of the airways) in patients with asthma or
COPD. Beta blockers should be used with caution in patients with these conditions,
and selective beta blockers (such as atenolol, metoprolol, and bisoprolol) are
generally preferred.
 Peripheral vascular disease: Beta blockers can worsen peripheral vascular disease,
a condition in which blood flow to the limbs is reduced. Beta blockers should be
used with caution in patients with peripheral vascular disease.

Contraindication
 Diabetes: Beta blockers can mask the symptoms of
hypoglycemia (low blood sugar) in patients with diabetes. Beta
blockers should be used with caution in patients with diabetes,
and blood sugar should be closely monitored.
 Pregnancy: Beta blockers can cross the placenta and may
affect fetal heart rate and blood sugar levels. Beta blockers
should be used with caution in pregnancy, and the benefits
and risks should be carefully weighed.
 Allergy or hypersensitivity: Patients with a known allergy or
hypersensitivity to beta blockers should not use these
medications.

Classification of
antihypertensive agent
 Calcium channel blocker MOA:
 here are two main types of CCBs: dihydropyridine and non-
dihydropyridine.
 Dihydropyridine CCBs, such as nifedipine and amlodipine, have
greater effects on the smooth muscle of blood vessels, resulting in
vasodilation and reduced blood pressure.
 Non-dihydropyridine CCBs, such as verapamil and diltiazem, have
greater effects on the heart, including slowing of conduction
through the AV node and reducing myocardial contractility.

agent
 Calcium channel blocker MOA:
 Calcium channel blockers (CCBs) are a class of medications that work by blocking the influx of
calcium ions into cells, which can lead to relaxation of smooth muscle and reduced
contractility of the heart. CCBs selectively inhibit L-type voltage-gated calcium channels,
which are predominantly found in cardiac and smooth muscle cells.
 The mechanism of action of CCBs involves binding to the alpha-1 subunit of the L-type
calcium channel, which reduces the influx of calcium ions into the cell. This reduces the
amount of calcium available to bind to the contractile proteins in the smooth muscle cells and
cardiac myocytes, resulting in relaxation of the muscle and reduced contractility of the heart.

Indication of calcium channel
blocker and dosage
 calcium channel blockers (CCBs) have several indications
and are commonly used to treat hypertension, angina,
and certain arrhythmias. They may also be used in the
management of Raynaud's phenomenon, subarachnoid
hemorrhage, and migraines.
 The dosage of CCBs may vary depending on the specific
medication, the indication for use, and individual patient
factors such as age and comorbidities. Below are some
general dosages for commonly used CCBs:

Indication of calcium channel
blocker and dosage
 Dihydropyridine CCBs:
 Amlodipine: 2.5-10 mg once daily
 Nifedipine: 30-90 mg once daily
 Felodipine: 5-10 mg once daily
 Nicardipine: 20-40 mg every 8 hours
 Non-dihydropyridine CCBs:
 Verapamil: 80-240 mg once or twice daily
 Diltiazem: 60-360 mg once or twice daily

Side effect calcium channel
blocker
 Calcium channel blockers (CCBs) are generally well-tolerated
medications, but like all medications, they can have side effects.
Some common side effects of CCBs include:
 Dizziness or lightheadedness
 Flushing
 Headache
 Swelling in the legs or ankles
 Constipation
 Slow heart rate
 Low blood pressure

Side effect calcium channel
blocker
 In rare cases, CCBs may also cause more serious side
effects, such as:
 Allergic reactions, including difficulty breathing or
swelling of the face, lips, tongue, or throat
 Liver damage
 Heart failure or worsening of heart failure symptoms
 Abnormal heart rhythms
 Stevens-Johnson syndrome or toxic epidermal
necrolysis, which are rare but serious skin reactions

toxicity calcium channel blocker
 The toxicity of calcium channel blockers (CCBs) can cause
serious complications and can be life-threatening.
 Overdose of CCBs can lead to hypotension, bradycardia,
and various cardiovascular complications.

toxicity calcium channel blocker
 The following are some of the management strategies for CCB overdose:
 Activated charcoal administration: Activated charcoal may be given within
1-2 hours of ingestion to reduce the absorption of the drug.
 Intravenous fluids: Intravenous fluids can be administered to increase
blood pressure and improve organ perfusion.
 Vasopressors: In cases of severe hypotension, vasopressors like
norepinephrine, dopamine or epinephrine may be given to increase blood
pressure.
 Calcium infusion: Intravenous calcium infusion may be used to counteract
the effects of CCBs on the cardiovascular system. Calcium can also improve
contractility and increase heart rate.
 Glucagon administration: Glucagon is a hormone that can increase cardiac
contractility and heart rate. It may be administered intravenously to
improve cardiovascular function.
 Hemodialysis: Hemodialysis may be considered in cases of severe toxicity,
especially when the drug levels remain high despite other measures.

Contraindication
 Hypersensitivity: Patients with a known hypersensitivity to any calcium channel
blocker should not take the medication.
 Severe hypotension: CCBs may cause a drop in blood pressure, so they should be used
with caution in patients with severe hypotension or shock.
 Heart failure: CCBs may worsen heart failure symptoms, so they should be used with
caution or avoided in patients with severe heart failure.
 Bradycardia or heart block: CCBs may slow down the heart rate, so they should be
used with caution in patients with pre-existing bradycardia or heart block.
 Liver disease: CCBs may be metabolized in the liver, so they should be used with
caution in patients with liver disease.
 Pregnancy and breastfeeding: CCBs may cross the placenta and be excreted in breast
milk, so they should be used with caution in pregnant or breastfeeding women.

Classification of
 Angiotensin receptor blocker MOA:
 Angiotensin receptor blockers (ARBs) are a type of
medication used to treat hypertension (high blood
pressure) and heart failure.
 They work by blocking the action of angiotensin II, a
hormone that causes blood vessels to constrict,
increasing blood pressure.

Classification of
 Angiotensin II is produced by the body in response to
various stimuli, such as low blood pressure, low blood
volume, or activation of the renin-angiotensin-
aldosterone system (RAAS).
 When angiotensin II binds to its receptors on blood
vessels, it causes the vessels to narrow and the blood
pressure to increase. Angiotensin II also stimulates the
release of aldosterone, a hormone that causes the
kidneys to retain sodium and water, further increasing
blood volume and pressure.

Classification of
 ARBs work by selectively blocking the type 1 angiotensin II
receptor (AT1 receptor), which is responsible for the
vasoconstrictive and aldosterone-stimulating effects of
angiotensin II. By blocking the AT1 receptor, ARBs prevent
angiotensin II from exerting its effects, causing blood vessels to
relax and reducing blood pressure. ARBs also help to reduce
fluid retention and edema by reducing aldosterone secretion.

Indication of Angiotensin receptor
blockers and dosage
 some common indications for ARBs include:
 Hypertension: ARBs are often used as first-line treatment for
hypertension, especially in patients with diabetes or chronic kidney
disease.
 Heart failure: ARBs are used to improve symptoms and reduce the
risk of hospitalization in patients with heart failure.
 Diabetic nephropathy: ARBs can slow the progression of kidney
damage in patients with diabetes.
 Coronary artery disease: ARBs are used in combination with other
medications to reduce the risk of cardiovascular events in patients
with coronary artery disease.
 Stroke prevention: ARBs are sometimes used to prevent stroke in
patients with hypertension or other risk factors for stroke.

Indication of Angiotensin receptor
blockers and dosage
 Some commonly prescribed ARBs and their usual
dosages include:
 Losartan (Cozaar): 25-100 mg once daily
 Valsartan (Diovan): 80-320 mg once daily
 Candesartan (Atacand): 4-32 mg once daily
 Olmesartan (Benicar): 20-40 mg once daily
 Telmisartan (Micardis): 20-80 mg once daily

Side effect Angiotensin receptor
blockers and dosage
 Some of the most common side effects of ARBs include:
 Fatigue
 Headache
 Diarrhea
 Back pain or muscle cramps
 High potassium levels
 Low blood pressure
 Increased risk of infections
 Angioedema (a rare but serious allergic reaction that causes
swelling of the face, lips, tongue, throat, and/or extremities)

toxicity (ARBs) and management
overdose
 Angiotensin receptor blockers (ARBs) are generally safe
and well-tolerated, with a low risk of toxicity. However, in
cases of overdose or excessive use, ARBs can cause
toxicity and adverse effects.
 management should involve supportive care, including
close monitoring of vital signs, electrolyte levels, and
renal function. The patient should be placed in a supine
position, and their blood pressure should be monitored
frequently. In cases of severe hypotension or shock,
intravenous fluids or vasoconstrictors may be necessary
to maintain blood pressure.

Contraindication
 Pregnancy: ARBs can cause harm or even death to the developing fetus, so they are
contraindicated during pregnancy.
 Hypotension: ARBs can cause a drop in blood pressure, so they should be used with
caution in patients with hypotension or those at risk for hypotension.
 Hyperkalemia: ARBs can increase potassium levels in the blood, so they should be
used with caution in patients with hyperkalemia or those at risk for hyperkalemia.
 Renal artery stenosis: ARBs should not be used in patients with renal artery
stenosis, as they can worsen renal function.
 Allergy or hypersensitivity: Patients who have a known allergy or hypersensitivity
to ARBs should not take them.

agent
 Angiotensin converting enzyme inhibitor MOA :
 The mechanism of action of ACE inhibitors involves blocking the action of
angiotensin converting enzyme (ACE). ACE is an enzyme that plays a key role in the
renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and
fluid balance in the body.
 When blood pressure is low, the kidneys release the enzyme renin, which leads to
the production of angiotensin I. Angiotensin I is then converted to angiotensin II by
ACE. Angiotensin II is a potent vasoconstrictor, which means it causes blood vessels
to constrict, increasing blood pressure.
 ACE inhibitors block the action of ACE, which reduces the production of angiotensin
II and causes blood vessels to dilate, lowering blood pressure. In addition, ACE
inhibitors may also decrease the secretion of aldosterone, a hormone that
regulates sodium and fluid balance in the body.
 Overall, the mechanism of action of ACE inhibitors results in decreased vascular
resistance, improved blood flow, and decreased workload on the heart, making
them effective for the treatment of hypertension and heart failure.

Indication of (ACE)inhibitor and
dosage
 Angiotensin converting enzyme inhibitors (ACE inhibitors)
are primarily used for the treatment of hypertension
(high blood pressure) and heart failure. They are also
used for other conditions, such as diabetic nephropathy
(kidney disease caused by diabetes) and to prevent heart
attacks and strokes

Dosage:
 Enalapril: The starting dose for hypertension is usually 5 mg once daily,
which may be increased to a maximum of 40 mg per day. For heart failure,
the starting dose is usually 2.5 mg twice daily, which may be increased to a
maximum of 20 mg twice daily.
 Lisinopril: The starting dose for hypertension is usually 10 mg once daily,
the starting dose is usually 2.5 mg once daily, which may be increased to a
maximum of 20 mg once daily.
 Ramipril: The starting dose for hypertension is usually 2.5 mg once daily,
the starting dose is usually 1.25 mg once daily, which may be increased to a
maximum of 10 mg once daily.
 Captopril: The starting dose for hypertension is usually 25 mg three times
daily, which may be increased to a maximum of 450 mg per day. For heart
failure, the starting dose is usually 6.25 mg three times daily, which may be
increased to a maximum of 50 mg three times daily.

toxicity ACE inhibitors and
management over dose
 toxicity of ACE inhibitors can occur if the dosage is too
high or if they are taken in combination with other
medications that interact with them. The symptoms of
ACE inhibitor toxicity may include low blood pressure,
dizziness, fainting, headache, dry cough, kidney
dysfunction, and electrolyte imbalances.

Management
 Stabilization of vital signs: This includes monitoring and managing blood
pressure, heart rate, and respiratory rate.
 Gastric decontamination: If the ACE inhibitor was taken recently, gastric
decontamination may be performed to prevent further absorption of the
medication. This may involve induced vomiting or gastric lavage.
 Administration of activated charcoal: Activated charcoal may be given to
help absorb the medication and prevent its absorption into the
bloodstream.
 Supportive care: Supportive care may be necessary to manage symptoms
such as low blood pressure, electrolyte imbalances, and kidney
dysfunction. This may involve fluid replacement, electrolyte replacement,
and renal function monitoring.

Side effect ACE inhibitor
 Dry cough: This is a common side effect of ACE inhibitors, affecting
up to 20% of patients. The cough can be persistent and may require
discontinuation of the medication.
 Hypotension: ACE inhibitors can cause a drop in blood pressure,
which may cause dizziness, lightheadedness, or fainting.
 Hyperkalemia: ACE inhibitors can cause an increase in potassium
levels in the blood, which may cause weakness, fatigue, or irregular
heartbeat.
 Angioedema: In rare cases, ACE inhibitors can cause swelling of the
face, lips, tongue, or throat, which can be life-threatening.
 Renal dysfunction: ACE inhibitors can affect kidney function,
especially in patients with preexisting kidney disease.
 Skin rash: Some individuals may develop a skin rash or itching while
taking ACE inhibitors.

Contraindication
 Pregnancy: ACE inhibitors can cause harm to the fetus if taken during pregnancy,
especially during the second and third trimesters. They are contraindicated in
pregnant women and women who are planning to become pregnant.
 Hypotension: ACE inhibitors can cause a drop in blood pressure, which may be
dangerous in individuals with severe hypotension or shock.
 Renal artery stenosis: ACE inhibitors may decrease blood flow to the kidneys and
worsen kidney function in patients with renal artery stenosis.
 Hyperkalemia: ACE inhibitors can cause an increase in potassium levels in the
blood, which may be dangerous in individuals with preexisting hyperkalemia.
 Angioedema: Individuals who have experienced angioedema or swelling of the
face, lips, tongue, or throat in response to ACE inhibitors or other medications in
the same class should not take ACE inhibitors.

Classification of
 Direct arterial vasodilator
 The mechanism of action (MOA) of direct arterial vasodilators
involves the activation of guanylate cyclase enzyme in the smooth
muscle cells of the arteries. This enzyme catalyzes the conversion of
guanosine triphosphate (GTP) to cyclic guanosine monophosphate
(cGMP).
 cGMP acts as a second messenger and causes relaxation of smooth
muscle cells by promoting the efflux of calcium ions from the
cytoplasm, which reduces the sensitivity of the contractile proteins
to calcium ions, leading to arterial dilation.
 Examples of direct arterial vasodilators include hydralazine,
minoxidil, and sodium nitroprusside.

Indication of Direct arterial
vasodilator and dosage
 Hydralazine:
 Indication: Used in the treatment of hypertension and heart failure,
particularly in patients with renal impairment.
 Dosage: Initial dose is usually 10 mg orally or intravenously, 3-4 times a day. The
maintenance dose is usually 25-50 mg orally, 3-4 times a day.
 Minoxidil:
 Indication: Used in the treatment of severe hypertension that is refractory to
other antihypertensive medications.
 Dosage: Initial dose is usually 5 mg orally once a day. The dose can be increased
gradually up to a maximum of 100 mg per day.
 Sodium Nitroprusside:
 Indication: Used in the treatment of hypertensive emergencies and severe
heart failure.
 Dosage: Usually administered intravenously, with an initial dose of 0.3-0.5
mcg/kg/min. The dose can be increased gradually up to a maximum of 10
mcg/kg/min.

toxicity Direct arterial vasodilator
and management over dose
 Hydralazine:
 Toxicity can cause headache, palpitations, tachycardia, nausea, vomiting, and
dizziness. Severe toxicity can lead to hypotension, reflex tachycardia, and
myocardial ischemia.
 Management: Supportive measures, such as monitoring vital signs and
administering intravenous fluids, may be necessary. In severe cases,
vasopressors and inotropic agents may be needed.
 Minoxidil:
 Toxicity can cause tachycardia, flushing, headache, and edema. Severe toxicity
can lead to hypotension, myocardial ischemia, and electrolyte imbalances.
 Management: Supportive measures, such as monitoring vital signs and
administering intravenous fluids, may be necessary. Electrolyte imbalances
should be corrected. In severe cases, vasopressors and inotropic agents may be
needed.
 Toxicity can cause hypotension, cyanide poisoning, and methemoglobinemia.
 Management: If toxicity is suspected, the drug should be immediately
discontinued, and the patient's vital signs should be closely monitored.
Cyanide poisoning can be treated with sodium thiosulfate, and
methemoglobinemia can be treated with methylene blue.

Side effect Direct arterial
vasodilator
Hydralazine:
Headache
Flushing
Dizziness
Palpitations
Tachycardia
Nausea and vomiting
Joint pain
Lupus-like syndrome (rare)
Muscle twitching

Side effect Direct arterial
vasodilator
 Minoxidil:
 Fluid retention
 Tachycardia
 Flushing
 Breast tenderness and enlargement (in men)
 Hirsutism (excessive hair growth)
 Electrolyte imbalances
 Hypotension
 Cyanide toxicity (rare)
 Methemoglobinemia (rare)
 Headache
 Nausea and vomiting
 Muscle twitching

contraindication
 Hydralazine:
 Hypersensitivity to hydralazine
 Mitral valve rheumatic heart disease
 Aortic dissection or dissecting aneurysm
 Coronary artery disease or angina pectoris
 Systemic lupus erythematosus
 Minoxidil:
 Hypersensitivity to minoxidil
 Pheochromocytoma
 Aortic dissection or dissecting aneurysm
 Acute myocardial infarction
 Severe renal impairment
 Hypersensitivity to sodium nitroprusside
 Severe hypotension or shock
 Increased intracranial pressure
 Co-administration with phosphodiesterase inhibitors (e.g., sildenafil)

agent
 Sympatholytic and adrenergic blocker MOA:
 sympatholytic drugs, such as alpha-adrenergic agonists or
centrally-acting sympatholytic, act on various sites in the
body to inhibit the release or uptake of norepinephrine, a
neurotransmitter that activates the sympathetic nervous
system. By reducing the amount of norepinephrine that is
available to bind to its receptors, sympatholytic drugs
decrease the overall level of sympathetic activity in the
body. This can result in a decrease in blood pressure,
heart rate, and other physiological responses associated
with the "fight or flight" response

Classification of
 Adrenergic blockers, on the other hand, work by blocking the
effects of norepinephrine and other similar neurotransmitters.
There are two main types of adrenergic blockers: alpha
blockers and beta blockers. Alpha blockers block the alpha
receptors, which are responsible for vasoconstriction and
increased blood pressure, while beta blockers block the beta
receptors, which are responsible for increased heart rate and
cardiac output. By blocking the effects of these
neurotransmitters, adrenergic blockers can decrease blood
pressure, heart rate, and other physiological responses
associated with sympathetic nervous system activity.

Cont.
 Overall, both sympatholytic drugs and adrenergic blockers
can be used to treat conditions such as hypertension,
heart failure, and anxiety by reducing sympathetic activity
and blocking the effects of norepinephrine and other
sympathetic neurotransmitters.


Indication of Sympatholytic and
adrenergic blocker and dosage
 Some examples of sympatholytic and adrenergic blocker drugs,
along with their dosages, are:
 Clonidine (sympatholytic): Initial dose is 0.1 mg orally twice a day,
gradually increased by 0.1-0.2 mg every 3-7 days as needed.
Maximum dose is typically 2.4 mg/day.
 Guanfacine (sympatholytic): Initial dose is 1 mg orally once a day,
gradually increased by 1 mg every 3-7 days as needed. Maximum
dose is typically 4 mg/day.
 Prazosin (adrenergic blocker): Initial dose is 1 mg orally two or three
times a day, gradually increased by 1-2 mg every 3-7 days as needed.
Maximum dose is typically 20 mg/day.
 Doxazosin (adrenergic blocker): Initial dose is 1 mg orally once a day,
gradually increased by 1-2 mg every 1-2 weeks as needed.
Maximum dose is typically 16 mg/day.

toxicity sympatholytic and adrenergic
blocker and management over dose
 Supportive care: The patient may be given fluids and electrolytes to
help manage their blood pressure and prevent dehydration.
 Activated charcoal: Activated charcoal may be given to help absorb
any remaining medication in the digestive system.
 Monitoring: The patient's vital signs, such as blood pressure, heart
rate, and respiratory rate, will be closely monitored to ensure they
remain stable.
 Specific antidotes: In severe cases, specific antidotes such as
glucagon, atropine, or norepinephrine may be given to counteract
the effects of the medication.
 Gastric lavage: In some cases, gastric lavage (stomach pumping)
may be necessary to remove any remaining medication from the
digestive system.

Side effect sympatholytic and
adrenergic blocker
 Some common side effects of these medications include:
 Dry mouth or eyes
 Constipation or diarrhea
 Sexual dysfunction
 Headache
 Insomnia or drowsiness
 Rash or itching
 Changes in blood pressure or heart rate.

Contraindication
 Some common contraindications for these medications include:
 Known hypersensitivity: Patients who are allergic to a specific sympatholytic or
adrenergic blocker medication should not take that drug.
 Cardiovascular disease: Patients with certain cardiovascular conditions, such as
severe bradycardia, heart block, or heart failure, may be contraindicated for these
medications.
 Pregnancy and breastfeeding: Some sympatholytic and adrenergic blocker
medications may be contraindicated for use during pregnancy or while
breastfeeding, due to potential risks to the developing fetus or nursing infant.
 Mental health disorders: Patients with certain mental health conditions, such as
depression or bipolar disorder, may be contraindicated for some of these
medications due to their potential to worsen these conditions.
 Other medical conditions: Patients with certain medical conditions, such as liver or
kidney disease, may be contraindicated for these medications due to their potential
to worsen these conditions or interact with other medications

The antihypertensive potential of flavonoids from Chinese
Herbal Medicine: A review
Cao, Y., Xie, L., Liu, K., Liang, Y., Dai, X., Wang, X., ... & Li, X. (2021). The antihypertensive potential of
flavonoids from Chinese Herbal Medicine: A review. Pharmacological Research, 174, 105919.
 Abstract
 With the coming of the era of the aging population, hypertension has become a global
health burden to be dealt with. Although there are multiple drugs and procedures to
control the symptoms of hypertension, the management of it is still a long-term
process, and the side effects of conventional drugs pose a burden on
patients. Flavonoids, common compounds found in fruits and vegetables as
secondary metabolites, are active components in Chinese Herbal Medicine. The
flavonoids are proved to have cardiovascular benefits based on a plethora of animal
experiments over the last decade. Thus, the flavonoids or flavonoid-rich plant extracts
endowed with anti-hypertension activities and probable mechanisms were reviewed. It
has been found that flavonoids may affect blood pressure in various ways. Moreover,
despite the substantial evidence of the potential for flavonoids in the control of
hypertension, it is not sufficient to support the clinical application of flavonoids as an
adjuvant or core drug. So the synergistic effects of flavonoids with other
drugs, pharmacokinetic studies, clinical trials and the safety of flavonoids are also
incorporated in the discussion. It is believed that more breakthrough studies are
needed. Overall, this review may shed some new light on the explicit recognition of the
mechanisms of anti-hypertension actions of flavonoids, pointing out the limitations of
relevant research at the current stage and the aspects that should be strengthened in
future researches.(Cao, Y., Xie, L., Liu, K., Liang, Y., Dai, X., Wang, X., ... & Li, X. (2021).

CONT…..
 Recent data from the global disease burden project shown that
elevated blood pressure remains the largest single contributor to
the global disease burden and global mortality, which increases
morbidity and mortality of cardiovascular and kidney diseases
[1]. Intensive antihypertensive drug therapy for patients should
be adopted as a supplementary method of primary prevention to
reduce the prevalence of blood pressure-related cardiovascular
diseases (CVD) and premature deaths [2], [3], [4]. It is predicted
that the prevalence of hypertension will increase globally from
2000 to 2025 due to the growing aging population [5]. However,
about three-quarters of patients with hypertension are living in
low- and middle-income countries, where the health literacy, the
level of medical treatment or the management of hypertension is
much more inferior than that in high-income countries [6]

CONT….
 The front-line antihypertensive drugs recommended by the World
Health Organization (WHO) include diuretics, β receptor blockers,
calcium antagonists, angiotensin-transferase inhibitors, and
angiotensin II receptor antagonists. The antihypertensive effect of
these drugs is strong and effective, but they have many adverse
reactions, such as elevated blood lipids, water and sodium retention,
ankle swelling, cough, redness, and vertigo [7], [8]. Furthermore,
these drugs cannot meet the needs of long-term use and the
improvement of the symptoms of hypertension. There are some
reports in recent years on resistant hypertension patients, with an
estimated 10–20% of hypertensive patients considered resistant to
treatment. These patients used three drugs, including diuretics, but
the blood pressure was still uncontrolled at the maximum tolerated
dosage. Some of them even used four drugs to control blood
pressure [9]. Therefore, the development of novel drugs for the
treatment and prevention of hypertension becomes more important.

CONT….
 Chinese Herbal Medicine (CHM) has its unique advantages in
treating hypertension. In China, CHM is widely used clinically as one
of the treatment methods. It can exert a good effect on treating
hypertension and at the same time, reduce the prevalence of
complications associated with metabolic abnormalities [10], which
indicates that CHM may have a great potential in the prevention and
treatment of hypertension. Flavonoids, a class of polyphenol
antioxidants, are the main active components in many CHM such
as Alismatis rhizoma, Achyranthis bidentate radix, Amomi
fructus, Andrographis herba, and Platycladi cacumen [11], [12].
Modern pharmacology has shown that flavonoids have significant
efficacy in improving cardiovascular function, preventing and treating
hypertension [13], [14]. This work aims to systematically review the
evidence on the effect of supplementation with flavonoids-rich herbs
and flavonoids supplements on hypertension in humans over the
past decade.

CONT…..
 The classification, the herbal origin and the determination of flavonoids in
CHM
 Flavonoids are found in a wide range of sources and are very important
organic compounds in nature. Most plants contain flavonoids, which play an
extremely important role in the growth of plants. Flavonoids in plants are
mostly in the form of glycosides, partly in free form. These compounds
possess a 2-phenylchromanone (flavone) structure with a 15-carbon
skeleton consisting of two phenyl rings named A and B, connected by
heterocyclic 4H-pyran rings named C (Fig. 1). Flavonoids also include
 Flavones
 Flavones are widely found in CHM, such as Scutellariae
Radix, Chrysanthemi flos. In recent years, the main flavonoids reported
having antihypertensive effects are apigenin, chrysin, diosmetin, linarin, and
luteolin.
 Apigenin, a widespread dietary flavone, can significantly reduce elevated
blood pressure levels in mice due to chronic L-NAME administration. This
effect was accompanied by a normalization of the reduced vascular reactivity
to vasoconstrictors and lower sodium retention. An enhanced

CONT….
 Discussion
 As is stated above, flavonoids have been proved to be powerful candidates
for improving hypertension and its complications. The regulation mechanism
of blood pressure in the human body is very complex, which can be divided
into nerve regulation, humoral regulation, and cardiovascular regulation.
Clinically, the occurrence of hypertension must involve the dysfunction of
multiple systemic tissues. The antihypertensive mechanisms of flavonoids
are mostly similar, such as the antioxidative effect
 Conclusions and expectations
 This review primarily focuses on the regulatory effects of flavonoids from
CHM in terms of hypertension and complications. Based on the findings, we
consider that flavonoids have the potential as an alternative approach for the
treatment of hypertension clinically.
 In spite of exhibiting diverse bioactivity, flavonoids are yet to become
promising drug candidates, and only a few of these compounds have been
approved for clinical application. Lacking sufficient clinical in vivo data may
be one of

References
 Cao, Y., Xie, L., Liu, K., Liang, Y., Dai, X., Wang, X., ... & Li, X. (2021). The antihypertensive potential of
flavonoids from Chinese Herbal Medicine: A review. Pharmacological Research, 174, 105919.
 Barbé, F., Durán-Cantolla, J., Capote, F., de la Peña, M., Chiner, E., Masa, J. F., ... & Montserrat, J. M.
(2010). Long-term effect of continuous positive airway pressure in hypertensive patients with sleep
apnea. American journal of respiratory and critical care medicine, 181(7), 718-726.
 Joshi, V. D., Dahake, A. P., & Suthar, A. P. (2010). Adverse effects associated with the use of
antihypertensive drugs: An overview. Int. J. Pharm. Tech. Res, 2, 10-13.
 Law, M., Wald, N., & Morris, J. (2003). Lowering blood pressure to prevent myocardial infarction and
stroke: a new preventive strategy. Health technology assessment (Winchester, England), 7(31), 1-94.
 Appelros, P., Nydevik, I., Seiger, A., & Terént, A. (2002). Predictors of severe stroke: influence of
preexisting dementia and cardiac disorders. Stroke, 33(10), 2357-2362.
 Basic and clinical pharmacology 15th edition

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