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Dr. Hiwa K. Saaed
PhD Pharmacology & Toxicology
2015-16
Reference: Lippincott illustrated Reviews of Pharmacology 6th ed.
Antihypertensives
Cardiovascular
Pharmacology
Classification for the purpose of RX
Category Systolic Blood
Pressure
Diastolic Blood
Pressure
Normal < 120 <80
Pre-hypertension 120-139 80-89
Hypertension – Stage 1 140-159 90-99
Hypertension – Stage 2 >160 >100
Hypertension (BP >140/90 mm Hg)
is defined as either a sustained SBP of > 140 mm Hg or a
sustained DBP of > 90 mm Hg.)
Optimal healthy blood pressure is (<120/<80).
Hypertension
INCIDENCE
• Elevated blood pressure is a common disorder,
affecting approximately 30% of adults in the United
States.
• Although many patients have no symptoms, chronic
hypertension can lead to heart disease and stroke, the
top two causes of death in the world.
• Hypertension is also an important risk factor in the
development of chronic kidney disease and heart
failure.
Primary or essential
(idiopathic) HTN >90% of all
cases.
Risks Factors include:
• Hyperlipidemia
• Diabetes
• Genetic, Family History
• sex (males are at higher risk)
• Race (4X black than whites)
• Age
• Obesity
• Stressful life style
• cigarette smoking
• High dietary intake of Na+
Secondary HTN (~10% of all
cases)
Identifiable Cause:
• Renal Artery
Constriction
• Coarctation of the Aorta
• Phaeochromocytoma
• Cushing’s Disease
• Primary Aldosteronism
• Drugs
Etiology of HTN
HOW TO TREAT HYPERTENSION?
I. NON-PHARMACOLOGICAL
– Quitting cigarette smoking,
– regular exercise,
– restricting dietary intake of: salt, saturated fats, and
calories
will improve peripheral circulation, prevent increases in blood
volume, reduce plasma cholesterol levels and total body
weight.
ANTIHYPERTENSIVE DRUGS
• Thiazide diuretics: (bendroflumethiazide)
• β-adrenoreceptor antagonists: (propranolol, atenolol,
metoprolol)
• Calcium channel antagonists: (nifedipine, amlodipine)
• Angiotensin converting enzyme (ACE) inhibitors: (captopril,
enalapril)
• Angiotensin II subtype I (AT1) receptor antagonists (losartan,
valsartan)
• Renin synthesis inhibitor: (Aliskiren)
• α1 adrenoreceptor antagonists: (prazosin, terazosin)
• Vasodilator drugs e.g. K+ channel activators: minoxidil
• Centrally-acting drugs e.g. α2 adrenoreceptor agonists:
(clonidine, methyldopa)
TREATMENT STRATEGIES
• For most patients, the blood pressure goal when treating
hypertension is a SBP<140 mm Hg and a DBP< 90 mm Hg.
• Mild hypertension can sometimes be controlled with
monotherapy, but most patients require more than one drug to
achieve blood pressure control.
• Current recommendations are:
– to initiate therapy with a thiazide diuretic, ACE inhibitor, angiotensin
receptor blocker (ARB), or calcium channel blocker (CCB).
– if blood pressure is inadequately controlled, a second drug should be
added.
A. Individualized care
 Black patients respond well to diuretics and CCBs, but
therapy with β-blockers or ACE inhibitors is often less
effective.
 Elderly respond well to CCBs, ACE inhibitors, and diuretics
are favored for treatment of hypertension in the elderly,
whereas β-blockers and α-antagonists are less well tolerated.
Initiating and titrating antihypertensive
Frequency of occurrence of concomitant
disease among the hypertensive population
Patient compliance in antihypertensive
therapy
• Lack of patient compliance is the most common reason for
failure of antihypertensive therapy.
• The hypertensive patient is usually asymptomatic. Thus,
therapy is generally directed at preventing future disease
sequelae rather than relieving current discomfort.
• The adverse effects associated with the hypertensive therapy
may influence the patient more than the future benefits.
• For example, β-blockers can cause sexual dysfunction in
males, which may prompt discontinuation of therapy.
• Thus, it is important to enhance compliance by
– selecting a drug regimen that reduces adverse effects
– minimizes the number of doses required daily.
– Combining two drug classes in a single pill, at a fixed-dose
combination.
Normal regulation of blood pressure (BP)
 Arterial blood pressure is regulated within a narrow range to provide adequate
perfusion of the tissues without causing damage to the vascular system, particularly
the arterial intima (endothelium).
 Arterioles: peripheral resistance.
 The CO depends on the stroke volume (SV) and the heart rate (HR).
 The main factors affecting SV are: the plasma volume and the venous return.
 HR is controlled primarily by sympathetic nerves (increase heart rate) and
parasympathetic nerves (decrease heart rate).
Mechanisms for Controlling Blood
Pressure
• In both normal and hypertensive individuals, cardiac output
and peripheral resistance are controlled mainly by two
overlapping control mechanisms:
– Baroreflexes, which are mediated by the sympathetic nervous system
– Reninangiotensin-aldosterone system (RAAS)
• Most antihypertensive drugs lower blood pressure by
reducing
• cardiac output and/or decreasing peripheral resistance.
A. Baroreceptor reflex arch
• Baroreflexes involving the sympathetic nervous system are
responsible for the rapid, moment-to-moment regulation of
blood pressure.
• A fall in blood pressure causes pressure-sensitive neurons
(baroreceptors in the aortic arch and carotid sinuses) to send
fewer impulses to cardiovascular centers in the spinal cord.
• This prompts a reflex response of increased sympathetic and
decreased parasympathetic output to the heart and
vasculature, resulting in vasoconstriction and increased
cardiac output.
• These changes result in a compensatory rise in blood pressure
Baroreceptor reflex arch
B. Renin–angiotensin–aldosterone
system
• Kidney provides for long-term control of blood pressure by altering
blood volume.
• Baroreceptors in kidney respond to reduced arterial pressure (and
to sympathetic stimulation of adrenoceptors) by releasing the
enzyme renin.
• This peptidase converts angiotensinogen to angiotensin I, which is
converted in turn to angiotensin II in presence of (ACE).
• Angiotensin II is the body's most potent circulating vasoconstrictor,
causing an increase in blood pressure.
• Furthermore, angiotensin II stimulates aldosterone secretion,
leading to increased renal sodium reabsorption and increased blood
volume, which contribute to a further increase in blood pressure.
Mechanisms for Controlling Blood
Pressure
Drug Targets for Controlling Blood
Pressure
Diuretics
A. Thiazide diuretics
B. Loop diuretics
C. Potassium-sparing diuretics
• Diuretics are currently recommended as the first-line drug
therapy for hypertension unless there are compelling reasons
to chose another agent.
• Low-dose diuretic therapy is safe and effective in preventing
stroke, myocardial infarction, and congestive heart failure, all
of which can cause mortality.
• Recent data suggest that diuretics are superior to β-blockers in
older adults.
A. Thiazide
actions
• Thiazides have found the most widespread
use. Thiazide diuretics decrease BP in both
supine and standing positions.
• These agents counteract the sodium and
water retention observed with other agents
used in treatment of hypertension (e.g,
hydralazine).
Actions: Thiazide diuretics lower BP initially
by increasing sodium and water excretion.
This causes a decrease in extracellular volume,
resulting in a decrease in cardiac output .
• With long-term treatment, plasma volume
approaches a normal value, but peripheral
resistance decreases.
Thiazide therapeutic uses
• Thiazides are useful in combination therapy with β- blockers
and ACE inhibitors. Thiazide diuretics are useful in the
treatment of black or elderly patients.
• They are not effective in patients with inadequate kidney
function (creatinine clearance <50 mL/min). Loop diuretics may
be required in these patients.
• Spironolactone, a potassium sparing diuretic, is used with
thiazides. Spironolactone has the additional benefit of
diminishing the cardiac remodeling that occurs in heart failure.
B. Loop diuretics
• The loop diuretics act promptly, even in patients with poor
renal function or who have not responded to thiazides or other
diuretics.
• The loop diuretics cause decreased renal vascular resistance
and increased renal blood flow.
C. Potassium-sparing
diuretics
• Amiloride and triamterene (inhibitors of epithelial sodium
transport at the late distal and collecting ducts)
• spironolactone and eplerenone (aldosterone receptor
antagonists) reduce potassium loss in the urine.
• Aldosterone antagonists have the additional benefit of
diminishing the cardiac remodeling that occurs in heart failure.
• Potassium-sparing diuretics are sometimes used in
combination with loop diuretics and thiazides to reduce the
amount of potassium loss induced by these diuretics.
β-Adrenoceptor-blocking Agents
β-Blockers are currently recommended as first-line drug therapy for
hypertension when indicated-for example, with heart failure.
A. Actions
• The Beta-blockers reduce BP primarily by decreasing cardiac
output. They may also decrease sympathetic outflow from CNS and
inhibit the release of renin from the kidneys, thus decreasing the
formation of angiotensin II and secretion of aldosterone.
• Prototype β-blocker is propranolol, which acts at both β1 and β2
receptors.
• Selective blockers of β1 receptors, such as metoprolol and atenolol, are
among the most commonly prescribed β-blockers.
• The selective β-blockers may be administered cautiously to hypertensive
patients who also have asthma, for which propranolol is contraindicated
due to its blockade of β2-mediated bronchodilation.
β-Adrenoceptor blockers
B. Therapeutic uses
• The β-blockers are orally active. The β-blockers may take several
weeks to develop their full effects.
• The β-blockers are more effective for treating hypertension in white
than in black patients, and in young compared to elderly patients.
• Conditions that discourage the use of β-blockers (for example,
severe chronic obstructive lung disease, chronic congestive heart
failure, or severe symptomatic occlusive peripheral vascular
disease) are more commonly found in the elderly and in diabetics.
• Hypertensive patients with concomitant diseases: The β-blockers
are useful in treating conditions that may coexist with hypertension,
such as supraventricular tachyarrhythmia, previous myocardial
infarction, angina pectoris, chronic heart failure, and migraine
headache.
Adverse effects
Bradycardia, fatigue, lethargy, insomnia, and
hallucinations, hypotension, decrease libido,
impotence. Drug-induced sexual dysfunction can
severely reduce patient compliance.
Decrease HDL and increase plasma triacylglycerol.
Drug withdrawal: Abrupt withdrawal may cause
rebound hypertension, probably as a result of up-
regulation of β-receptors.
Used cautiously in the treatment of patients with
asthma, acute heart failure, or peripheral vascular
disease.
ACE Inhibitors
The ACE inhibitors, such as enalapril or lisinopril, are
recommended when the preferred first-line agents (diuretics or β-
blockers) are contraindicated or ineffective.
Actions
The ACE inhibitors lower blood pressure by reducing peripheral
vascular resistance without reflexively increasing cardiac output,
rate, or contractility.
These drugs block the ACE that
– cleaves AngI to form the potent vasoconstrictor AngII
– breakdown of bradykinin.
By reducing circulating angiotensin II levels, also decrease the
secretion of aldosterone, resulting in decreased sodium and water
retention.
ACE Inhibitors
Therapeutic uses
• Like β-blockers, ACE inhibitors are most effective in
hypertensive patients who are white and young. However,
when used in combination with a diuretic, the effectiveness of
ACE inhibitors is similar in white and black patients with
hypertension.
• Along with the angiotensin receptor blockers, ACE inhibitors
slow the progression of diabetic nephropathy and decrease
albuminuria.
• ACE inhibitors are also effective in the management of
patients with chronic heart failure.
• ACE inhibitors are a standard in the care of a patient following
a myocardial infarction.
Adverse effects
• Common side effects include dry cough, rash, fever,
altered taste, hypotension (in hypovolemic states), and
hyperkalemia.
• The dry cough, which occurs in about 10% of patients, is
thought to be due to increased levels of bradykinin in the
pulmonary tree.
• Potassium levels must be monitored, and potassium
supplements or spironolactone are contraindicated.
• Angioedema is a rare but potentially life-threatening
reaction and may also be due to increased levels of
bradykinin.
• Because of the risk of angioedema and first-dose syncope,
ACE inhibitors are first administered in the physician's
office with close observation.
• Reversible renal failure can occur in patients with severe
renal artery stenosis.
• ACE inhibitors are fetotoxic and should not be used by
women who are pregnant.
Angiotensin II-receptor Antagonists
• The Ang- II-receptor blockers (ARBs) are alternatives to the
ACE inhibitors.
• Losartan, is the prototypic ARB; currently, there are six
additional ARBs. Their pharmacologic effects are similar to
those of ACE inhibitors in that they produce vasodilation and
block aldosterone secretion, thus lowering blood pressure and
decreasing salt and water retention.
• ARBs decrease the nephrotoxicity of diabetes, making them an
attractive therapy in hypertensive diabetics.
• Their adverse effects are similar to those of ACE inhibitors,
although the risks of cough and angioedema are significantly
decreased. They are fetotoxic.
Calcium Channel Blockers (CCB)
• CCBs are recommended when the preferred first line agents
are contraindicated or ineffective.
• They are effective in treating hypertension in patients with
angina or diabetes.
• High doses of short-acting CCBs should be avoided because of
increased risk of myocardial infarction.
Classes of calcium channel blockers
• Verapamil
• Diltiazem
• Dihydropyridines (nifedipine, amlodipine, felodipine,
isradipine, nicardipine, and nisoldipine)
NonDihydropyridines CCB
• Verapamil is the least selective of any CCB, and has
significant effects on both cardiac and vascular smooth muscle
cells. It is used to treat angina, supraventricular
tachyarrhythmias, and migraine headache.
• Diltiazem, like verapamil, diltiazem affects both cardiac and
vascular smooth muscle cells; however, it has a less
pronounced negative inotropic effect on heart compared to that
of verapamil. Diltiazem has a favorable side-effect profile.
Dihydropyridines CCB
• Dihydropyridines include nifedipine, amlodipine, felodipine,
isradipine, nicardipine, and nisoldipine.
• These new-generation calcium channel blockers differ in
pharmacokinetics, approved uses, and drug interactions.
• All dihydropyridines have a much greater affinity for vascular
calcium channels than for calcium channels in the heart. They
are therefore particularly attractive in treating hypertension.
• Newer agents, such as amlodipine and nicardipine, have the
advantage that they show little interaction with other
cardiovascular drugs, such as digoxin or warfarin, which are
often used concomitantly with calcium channel blockers.
CCB Actions and uses
Actions: CCB block the inward movement of calcium by binding to L-
type calcium channels in the heart and in smooth muscle of the coronary
and peripheral vasculature. This causes vascular smooth muscle to relax,
dilating mainly arterioles.
Therapeutic uses
 Calcium channel blockers have an intrinsic natriuretic effect and, therefore,
do not usually require the addition of a diuretic.
 These agents are useful in the treatment of hypertensive patients who also
have asthma, diabetes, angina, and/or peripheral vascular disease.
 Black hypertensives respond well to calcium channel blockers.
• Most of these agents have short half-lives (3-8 hours). Treatment is
required three times a day to maintain good control of hypertension.
Therapeutic Indications of CCBs
Adverse effects of CCBs
Dihydrpyridines:
 Dizziness, headache, and a feeling of fatigue
caused by a decrease in blood pressure.
 Peripheral edema is another commonly
reported side effect of this class.
 Nifedipine and other dihydropyridines may
cause gingival hyperplasia.
Verapamil and diltiazem
Constipation and AV block, should be avoided
in patients with heart failure or with AV block.
Alpha(α )-Adrenoceptor-blocking Agents
• Prazosin, doxazosin, and terazosin: They decrease the PVR and
lower the arterial BP by causing relaxation of both arterial and
venous smooth muscle.
• These drugs cause only minimal changes in cardiac output,
renal blood flow, and glomerular filtration rate. Therefore, long-
term tachycardia does not occur, but salt and water retention
does.
Adverse effects:
• Postural hypotension may occur in some individuals.
• Reflex tachycardia (beta-blocker may be necessary to blunt the short-term
effect of reflex tachycardia).
• First-dose syncope are almost universal adverse effects.
Centrally Acting Adrenergic Drugs
Clonidine: α2 agonist diminishes central adrenergic outflow.
• Clonidine is used primarily for the treatment of mild to
moderate hypertension that has not responded adequately to
treatment with diuretics alone.
• Clonidine does not decrease renal blood flow or glomerular
filtration and, therefore, is useful in the treatment of
hypertension complicated by renal disease.
• Because it causes sodium and water retention, clonidine is
usually administered in combination with a diuretic.
• Side effects: mild (sedation, drying nasal mucosa)
• Rebound HT occurs following abrupt withdrawal of clonidine
α-Methyldopa
• α-Methyldopa: α2 agonists converted to
methylnorepinephrine centrally to diminish the adrenergic
outflow from the CNS, leading to reduced total peripheral
resistance and a decreased blood pressure.
• Cardiac output is not decreased and blood flow to vital
organs is not diminished. Because blood flow to the
kidney is not diminished by its use, α-methyldopa is
especially valuable in treating HT patients with renal
insufficiency.
• Side effects : sedation and drowsiness.
Vasodilators
 Direct-acting smooth muscle relaxants: hydralazine, minoxidil.
 Vasodilators produce relaxation of vascular smooth muscle,
which decreases resistance and therefore decreases blood
pressure.
 These agents produce reflex stimulation of the heart, resulting in
the competing symptoms of increased myocardial contractility,
heart rate, and oxygen consumption. These actions may prompt
angina pectoris, myocardial infarction, or cardiac failure in
predisposed individuals.
 Vasodilators also increase plasma renin concentration, resulting in
sodium and water retention. These undesirable side effects can be
blocked by concomitant use of a diuretic and a beta-blocker.
Hydralazine
• Hydralazine is used to treat moderately severe HT. It is
almost always administered in combination with a beta-
blocker such as propranolol (to balance the reflex tachycardia)
and a diuretic (to decrease sodium retention). Together, the
three drugs decrease cardiac output, plasma volume, and
peripheral vascular resistance.
• A lupus-like syndrome can occur with high dosage, but it is
reversible on discontinuation of the drug.
Minoxidil
• Minoxidil: This drug causes dilation of resistance vessels
(arterioles) but not of capacitance vessels (venules).
• Minoxidil is administered orally for treatment of severe to
malignant hypertension that is refractory to other drugs.
• Minoxidil causes serious sodium and water retention, leading
to volume overload, edema, and congestive heart failure.
• Minoxidil treatment also causes hypertrichosis (growth of
body hair). This drug is now used topically to treat male
pattern baldness.
HTN Emergency
• Hypertensive emergency is a rare but life-
threatening situation in which the DBP is either
>150 mm Hg (with SBP >210 mm Hg) in an
otherwise healthy person,
or a DBP of 130 mm Hg in an individual with
preexisting complications, such as
encephalopathy, cerebral hemorrhage, left-
ventricular failure, or aortic stenosis.
• The therapeutic goal is to rapidly reduce blood
pressure.
• A.Sodium nitroprusside
• B. Labetalol
• C. Fenoldopam
• D. Nicardipine
HTN Emergency
A. Sodium nitroprusside
• is administered IV, is metabolized rapidly (half life of minutes) and
requires continuous infusion to maintain its hypotensive action.
• It is capable of reducing blood pressure in all patients regardless of
the cause of hypertension,
• acting equally on arterial and venous smooth muscle. It can reduce
cardiac preload.
• Adverse effects: hypotension caused by overdose. Nitroprusside
metabolism results in cyanide ion production.
• Although cyanide toxicity is rare, it can be effectively treated with an
infusion of sodium thiosulfate to produce thiocyanate, which is less
toxic and is eliminated by the kidneys.
[Note: Nitroprusside is poisonous if given orally because of its
hydrolysis to cyanide.]
HTN Emergency
B. Labetalol
• is both an (alpha- and a beta-blocker and is given as an IV bolus or
infusion.
• NO reflex tachycardia.
• The major limitation is a longer half-life, which precludes rapid titration.
• carries the contraindications of a nonselective beta- blocker.
C. Fenoldopam
• Fenoldopam is a peripheral dopamine-1 receptor agonist that is given as an
IV infusion.
• Unlike other parenteral antihypertensive agents, fenoldopam maintains or
increases renal perfusion while it lowers blood pressure, beneficial in
patients with renal insufficiency.
D. Nicardipine
• Nicardipine, a calcium channel blocker, can be given as an IV infusion.
• limitation is a long half-life
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Antihypertensive drugs 2015-16

  • 1. Dr. Hiwa K. Saaed PhD Pharmacology & Toxicology 2015-16 Reference: Lippincott illustrated Reviews of Pharmacology 6th ed. Antihypertensives Cardiovascular Pharmacology
  • 2. Classification for the purpose of RX Category Systolic Blood Pressure Diastolic Blood Pressure Normal < 120 <80 Pre-hypertension 120-139 80-89 Hypertension – Stage 1 140-159 90-99 Hypertension – Stage 2 >160 >100 Hypertension (BP >140/90 mm Hg) is defined as either a sustained SBP of > 140 mm Hg or a sustained DBP of > 90 mm Hg.) Optimal healthy blood pressure is (<120/<80). Hypertension
  • 3. INCIDENCE • Elevated blood pressure is a common disorder, affecting approximately 30% of adults in the United States. • Although many patients have no symptoms, chronic hypertension can lead to heart disease and stroke, the top two causes of death in the world. • Hypertension is also an important risk factor in the development of chronic kidney disease and heart failure.
  • 4. Primary or essential (idiopathic) HTN >90% of all cases. Risks Factors include: • Hyperlipidemia • Diabetes • Genetic, Family History • sex (males are at higher risk) • Race (4X black than whites) • Age • Obesity • Stressful life style • cigarette smoking • High dietary intake of Na+ Secondary HTN (~10% of all cases) Identifiable Cause: • Renal Artery Constriction • Coarctation of the Aorta • Phaeochromocytoma • Cushing’s Disease • Primary Aldosteronism • Drugs Etiology of HTN
  • 5. HOW TO TREAT HYPERTENSION? I. NON-PHARMACOLOGICAL – Quitting cigarette smoking, – regular exercise, – restricting dietary intake of: salt, saturated fats, and calories will improve peripheral circulation, prevent increases in blood volume, reduce plasma cholesterol levels and total body weight.
  • 6. ANTIHYPERTENSIVE DRUGS • Thiazide diuretics: (bendroflumethiazide) • β-adrenoreceptor antagonists: (propranolol, atenolol, metoprolol) • Calcium channel antagonists: (nifedipine, amlodipine) • Angiotensin converting enzyme (ACE) inhibitors: (captopril, enalapril) • Angiotensin II subtype I (AT1) receptor antagonists (losartan, valsartan) • Renin synthesis inhibitor: (Aliskiren) • α1 adrenoreceptor antagonists: (prazosin, terazosin) • Vasodilator drugs e.g. K+ channel activators: minoxidil • Centrally-acting drugs e.g. α2 adrenoreceptor agonists: (clonidine, methyldopa)
  • 7.
  • 8. TREATMENT STRATEGIES • For most patients, the blood pressure goal when treating hypertension is a SBP<140 mm Hg and a DBP< 90 mm Hg. • Mild hypertension can sometimes be controlled with monotherapy, but most patients require more than one drug to achieve blood pressure control. • Current recommendations are: – to initiate therapy with a thiazide diuretic, ACE inhibitor, angiotensin receptor blocker (ARB), or calcium channel blocker (CCB). – if blood pressure is inadequately controlled, a second drug should be added.
  • 9. A. Individualized care  Black patients respond well to diuretics and CCBs, but therapy with β-blockers or ACE inhibitors is often less effective.  Elderly respond well to CCBs, ACE inhibitors, and diuretics are favored for treatment of hypertension in the elderly, whereas β-blockers and α-antagonists are less well tolerated.
  • 10. Initiating and titrating antihypertensive
  • 11. Frequency of occurrence of concomitant disease among the hypertensive population
  • 12. Patient compliance in antihypertensive therapy • Lack of patient compliance is the most common reason for failure of antihypertensive therapy. • The hypertensive patient is usually asymptomatic. Thus, therapy is generally directed at preventing future disease sequelae rather than relieving current discomfort. • The adverse effects associated with the hypertensive therapy may influence the patient more than the future benefits. • For example, β-blockers can cause sexual dysfunction in males, which may prompt discontinuation of therapy. • Thus, it is important to enhance compliance by – selecting a drug regimen that reduces adverse effects – minimizes the number of doses required daily. – Combining two drug classes in a single pill, at a fixed-dose combination.
  • 13. Normal regulation of blood pressure (BP)  Arterial blood pressure is regulated within a narrow range to provide adequate perfusion of the tissues without causing damage to the vascular system, particularly the arterial intima (endothelium).  Arterioles: peripheral resistance.  The CO depends on the stroke volume (SV) and the heart rate (HR).  The main factors affecting SV are: the plasma volume and the venous return.  HR is controlled primarily by sympathetic nerves (increase heart rate) and parasympathetic nerves (decrease heart rate).
  • 14. Mechanisms for Controlling Blood Pressure • In both normal and hypertensive individuals, cardiac output and peripheral resistance are controlled mainly by two overlapping control mechanisms: – Baroreflexes, which are mediated by the sympathetic nervous system – Reninangiotensin-aldosterone system (RAAS) • Most antihypertensive drugs lower blood pressure by reducing • cardiac output and/or decreasing peripheral resistance.
  • 15. A. Baroreceptor reflex arch • Baroreflexes involving the sympathetic nervous system are responsible for the rapid, moment-to-moment regulation of blood pressure. • A fall in blood pressure causes pressure-sensitive neurons (baroreceptors in the aortic arch and carotid sinuses) to send fewer impulses to cardiovascular centers in the spinal cord. • This prompts a reflex response of increased sympathetic and decreased parasympathetic output to the heart and vasculature, resulting in vasoconstriction and increased cardiac output. • These changes result in a compensatory rise in blood pressure
  • 17. B. Renin–angiotensin–aldosterone system • Kidney provides for long-term control of blood pressure by altering blood volume. • Baroreceptors in kidney respond to reduced arterial pressure (and to sympathetic stimulation of adrenoceptors) by releasing the enzyme renin. • This peptidase converts angiotensinogen to angiotensin I, which is converted in turn to angiotensin II in presence of (ACE). • Angiotensin II is the body's most potent circulating vasoconstrictor, causing an increase in blood pressure. • Furthermore, angiotensin II stimulates aldosterone secretion, leading to increased renal sodium reabsorption and increased blood volume, which contribute to a further increase in blood pressure.
  • 18. Mechanisms for Controlling Blood Pressure
  • 19. Drug Targets for Controlling Blood Pressure
  • 20. Diuretics A. Thiazide diuretics B. Loop diuretics C. Potassium-sparing diuretics • Diuretics are currently recommended as the first-line drug therapy for hypertension unless there are compelling reasons to chose another agent. • Low-dose diuretic therapy is safe and effective in preventing stroke, myocardial infarction, and congestive heart failure, all of which can cause mortality. • Recent data suggest that diuretics are superior to β-blockers in older adults.
  • 21. A. Thiazide actions • Thiazides have found the most widespread use. Thiazide diuretics decrease BP in both supine and standing positions. • These agents counteract the sodium and water retention observed with other agents used in treatment of hypertension (e.g, hydralazine). Actions: Thiazide diuretics lower BP initially by increasing sodium and water excretion. This causes a decrease in extracellular volume, resulting in a decrease in cardiac output . • With long-term treatment, plasma volume approaches a normal value, but peripheral resistance decreases.
  • 22. Thiazide therapeutic uses • Thiazides are useful in combination therapy with β- blockers and ACE inhibitors. Thiazide diuretics are useful in the treatment of black or elderly patients. • They are not effective in patients with inadequate kidney function (creatinine clearance <50 mL/min). Loop diuretics may be required in these patients. • Spironolactone, a potassium sparing diuretic, is used with thiazides. Spironolactone has the additional benefit of diminishing the cardiac remodeling that occurs in heart failure.
  • 23. B. Loop diuretics • The loop diuretics act promptly, even in patients with poor renal function or who have not responded to thiazides or other diuretics. • The loop diuretics cause decreased renal vascular resistance and increased renal blood flow.
  • 24. C. Potassium-sparing diuretics • Amiloride and triamterene (inhibitors of epithelial sodium transport at the late distal and collecting ducts) • spironolactone and eplerenone (aldosterone receptor antagonists) reduce potassium loss in the urine. • Aldosterone antagonists have the additional benefit of diminishing the cardiac remodeling that occurs in heart failure. • Potassium-sparing diuretics are sometimes used in combination with loop diuretics and thiazides to reduce the amount of potassium loss induced by these diuretics.
  • 25. β-Adrenoceptor-blocking Agents β-Blockers are currently recommended as first-line drug therapy for hypertension when indicated-for example, with heart failure. A. Actions • The Beta-blockers reduce BP primarily by decreasing cardiac output. They may also decrease sympathetic outflow from CNS and inhibit the release of renin from the kidneys, thus decreasing the formation of angiotensin II and secretion of aldosterone. • Prototype β-blocker is propranolol, which acts at both β1 and β2 receptors. • Selective blockers of β1 receptors, such as metoprolol and atenolol, are among the most commonly prescribed β-blockers. • The selective β-blockers may be administered cautiously to hypertensive patients who also have asthma, for which propranolol is contraindicated due to its blockade of β2-mediated bronchodilation.
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  • 28. B. Therapeutic uses • The β-blockers are orally active. The β-blockers may take several weeks to develop their full effects. • The β-blockers are more effective for treating hypertension in white than in black patients, and in young compared to elderly patients. • Conditions that discourage the use of β-blockers (for example, severe chronic obstructive lung disease, chronic congestive heart failure, or severe symptomatic occlusive peripheral vascular disease) are more commonly found in the elderly and in diabetics. • Hypertensive patients with concomitant diseases: The β-blockers are useful in treating conditions that may coexist with hypertension, such as supraventricular tachyarrhythmia, previous myocardial infarction, angina pectoris, chronic heart failure, and migraine headache.
  • 29. Adverse effects Bradycardia, fatigue, lethargy, insomnia, and hallucinations, hypotension, decrease libido, impotence. Drug-induced sexual dysfunction can severely reduce patient compliance. Decrease HDL and increase plasma triacylglycerol. Drug withdrawal: Abrupt withdrawal may cause rebound hypertension, probably as a result of up- regulation of β-receptors. Used cautiously in the treatment of patients with asthma, acute heart failure, or peripheral vascular disease.
  • 30. ACE Inhibitors The ACE inhibitors, such as enalapril or lisinopril, are recommended when the preferred first-line agents (diuretics or β- blockers) are contraindicated or ineffective. Actions The ACE inhibitors lower blood pressure by reducing peripheral vascular resistance without reflexively increasing cardiac output, rate, or contractility. These drugs block the ACE that – cleaves AngI to form the potent vasoconstrictor AngII – breakdown of bradykinin. By reducing circulating angiotensin II levels, also decrease the secretion of aldosterone, resulting in decreased sodium and water retention.
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  • 33. Therapeutic uses • Like β-blockers, ACE inhibitors are most effective in hypertensive patients who are white and young. However, when used in combination with a diuretic, the effectiveness of ACE inhibitors is similar in white and black patients with hypertension. • Along with the angiotensin receptor blockers, ACE inhibitors slow the progression of diabetic nephropathy and decrease albuminuria. • ACE inhibitors are also effective in the management of patients with chronic heart failure. • ACE inhibitors are a standard in the care of a patient following a myocardial infarction.
  • 34. Adverse effects • Common side effects include dry cough, rash, fever, altered taste, hypotension (in hypovolemic states), and hyperkalemia. • The dry cough, which occurs in about 10% of patients, is thought to be due to increased levels of bradykinin in the pulmonary tree. • Potassium levels must be monitored, and potassium supplements or spironolactone are contraindicated. • Angioedema is a rare but potentially life-threatening reaction and may also be due to increased levels of bradykinin. • Because of the risk of angioedema and first-dose syncope, ACE inhibitors are first administered in the physician's office with close observation. • Reversible renal failure can occur in patients with severe renal artery stenosis. • ACE inhibitors are fetotoxic and should not be used by women who are pregnant.
  • 35. Angiotensin II-receptor Antagonists • The Ang- II-receptor blockers (ARBs) are alternatives to the ACE inhibitors. • Losartan, is the prototypic ARB; currently, there are six additional ARBs. Their pharmacologic effects are similar to those of ACE inhibitors in that they produce vasodilation and block aldosterone secretion, thus lowering blood pressure and decreasing salt and water retention. • ARBs decrease the nephrotoxicity of diabetes, making them an attractive therapy in hypertensive diabetics. • Their adverse effects are similar to those of ACE inhibitors, although the risks of cough and angioedema are significantly decreased. They are fetotoxic.
  • 36. Calcium Channel Blockers (CCB) • CCBs are recommended when the preferred first line agents are contraindicated or ineffective. • They are effective in treating hypertension in patients with angina or diabetes. • High doses of short-acting CCBs should be avoided because of increased risk of myocardial infarction. Classes of calcium channel blockers • Verapamil • Diltiazem • Dihydropyridines (nifedipine, amlodipine, felodipine, isradipine, nicardipine, and nisoldipine)
  • 37. NonDihydropyridines CCB • Verapamil is the least selective of any CCB, and has significant effects on both cardiac and vascular smooth muscle cells. It is used to treat angina, supraventricular tachyarrhythmias, and migraine headache. • Diltiazem, like verapamil, diltiazem affects both cardiac and vascular smooth muscle cells; however, it has a less pronounced negative inotropic effect on heart compared to that of verapamil. Diltiazem has a favorable side-effect profile.
  • 38. Dihydropyridines CCB • Dihydropyridines include nifedipine, amlodipine, felodipine, isradipine, nicardipine, and nisoldipine. • These new-generation calcium channel blockers differ in pharmacokinetics, approved uses, and drug interactions. • All dihydropyridines have a much greater affinity for vascular calcium channels than for calcium channels in the heart. They are therefore particularly attractive in treating hypertension. • Newer agents, such as amlodipine and nicardipine, have the advantage that they show little interaction with other cardiovascular drugs, such as digoxin or warfarin, which are often used concomitantly with calcium channel blockers.
  • 39. CCB Actions and uses Actions: CCB block the inward movement of calcium by binding to L- type calcium channels in the heart and in smooth muscle of the coronary and peripheral vasculature. This causes vascular smooth muscle to relax, dilating mainly arterioles. Therapeutic uses  Calcium channel blockers have an intrinsic natriuretic effect and, therefore, do not usually require the addition of a diuretic.  These agents are useful in the treatment of hypertensive patients who also have asthma, diabetes, angina, and/or peripheral vascular disease.  Black hypertensives respond well to calcium channel blockers. • Most of these agents have short half-lives (3-8 hours). Treatment is required three times a day to maintain good control of hypertension.
  • 41. Adverse effects of CCBs Dihydrpyridines:  Dizziness, headache, and a feeling of fatigue caused by a decrease in blood pressure.  Peripheral edema is another commonly reported side effect of this class.  Nifedipine and other dihydropyridines may cause gingival hyperplasia. Verapamil and diltiazem Constipation and AV block, should be avoided in patients with heart failure or with AV block.
  • 42. Alpha(α )-Adrenoceptor-blocking Agents • Prazosin, doxazosin, and terazosin: They decrease the PVR and lower the arterial BP by causing relaxation of both arterial and venous smooth muscle. • These drugs cause only minimal changes in cardiac output, renal blood flow, and glomerular filtration rate. Therefore, long- term tachycardia does not occur, but salt and water retention does. Adverse effects: • Postural hypotension may occur in some individuals. • Reflex tachycardia (beta-blocker may be necessary to blunt the short-term effect of reflex tachycardia). • First-dose syncope are almost universal adverse effects.
  • 43. Centrally Acting Adrenergic Drugs Clonidine: α2 agonist diminishes central adrenergic outflow. • Clonidine is used primarily for the treatment of mild to moderate hypertension that has not responded adequately to treatment with diuretics alone. • Clonidine does not decrease renal blood flow or glomerular filtration and, therefore, is useful in the treatment of hypertension complicated by renal disease. • Because it causes sodium and water retention, clonidine is usually administered in combination with a diuretic. • Side effects: mild (sedation, drying nasal mucosa) • Rebound HT occurs following abrupt withdrawal of clonidine
  • 44. α-Methyldopa • α-Methyldopa: α2 agonists converted to methylnorepinephrine centrally to diminish the adrenergic outflow from the CNS, leading to reduced total peripheral resistance and a decreased blood pressure. • Cardiac output is not decreased and blood flow to vital organs is not diminished. Because blood flow to the kidney is not diminished by its use, α-methyldopa is especially valuable in treating HT patients with renal insufficiency. • Side effects : sedation and drowsiness.
  • 45. Vasodilators  Direct-acting smooth muscle relaxants: hydralazine, minoxidil.  Vasodilators produce relaxation of vascular smooth muscle, which decreases resistance and therefore decreases blood pressure.  These agents produce reflex stimulation of the heart, resulting in the competing symptoms of increased myocardial contractility, heart rate, and oxygen consumption. These actions may prompt angina pectoris, myocardial infarction, or cardiac failure in predisposed individuals.  Vasodilators also increase plasma renin concentration, resulting in sodium and water retention. These undesirable side effects can be blocked by concomitant use of a diuretic and a beta-blocker.
  • 46. Hydralazine • Hydralazine is used to treat moderately severe HT. It is almost always administered in combination with a beta- blocker such as propranolol (to balance the reflex tachycardia) and a diuretic (to decrease sodium retention). Together, the three drugs decrease cardiac output, plasma volume, and peripheral vascular resistance. • A lupus-like syndrome can occur with high dosage, but it is reversible on discontinuation of the drug.
  • 47. Minoxidil • Minoxidil: This drug causes dilation of resistance vessels (arterioles) but not of capacitance vessels (venules). • Minoxidil is administered orally for treatment of severe to malignant hypertension that is refractory to other drugs. • Minoxidil causes serious sodium and water retention, leading to volume overload, edema, and congestive heart failure. • Minoxidil treatment also causes hypertrichosis (growth of body hair). This drug is now used topically to treat male pattern baldness.
  • 48. HTN Emergency • Hypertensive emergency is a rare but life- threatening situation in which the DBP is either >150 mm Hg (with SBP >210 mm Hg) in an otherwise healthy person, or a DBP of 130 mm Hg in an individual with preexisting complications, such as encephalopathy, cerebral hemorrhage, left- ventricular failure, or aortic stenosis. • The therapeutic goal is to rapidly reduce blood pressure. • A.Sodium nitroprusside • B. Labetalol • C. Fenoldopam • D. Nicardipine
  • 49. HTN Emergency A. Sodium nitroprusside • is administered IV, is metabolized rapidly (half life of minutes) and requires continuous infusion to maintain its hypotensive action. • It is capable of reducing blood pressure in all patients regardless of the cause of hypertension, • acting equally on arterial and venous smooth muscle. It can reduce cardiac preload. • Adverse effects: hypotension caused by overdose. Nitroprusside metabolism results in cyanide ion production. • Although cyanide toxicity is rare, it can be effectively treated with an infusion of sodium thiosulfate to produce thiocyanate, which is less toxic and is eliminated by the kidneys. [Note: Nitroprusside is poisonous if given orally because of its hydrolysis to cyanide.]
  • 50. HTN Emergency B. Labetalol • is both an (alpha- and a beta-blocker and is given as an IV bolus or infusion. • NO reflex tachycardia. • The major limitation is a longer half-life, which precludes rapid titration. • carries the contraindications of a nonselective beta- blocker. C. Fenoldopam • Fenoldopam is a peripheral dopamine-1 receptor agonist that is given as an IV infusion. • Unlike other parenteral antihypertensive agents, fenoldopam maintains or increases renal perfusion while it lowers blood pressure, beneficial in patients with renal insufficiency. D. Nicardipine • Nicardipine, a calcium channel blocker, can be given as an IV infusion. • limitation is a long half-life
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