Anti Hypertensives NEW

PHARMACOLOGY & THERAPEUTICS –II
PD-410
Dr. Auwais Ahmed Khan

Assistant Professor (Pharmacology)
Dow College of Pharmacy, DUHS, Karachi
1
DRUGS USED IN
HYPERTENSION
Dr. Auwais Ahmed Khan 2

What is Blood Pressure?
• Blood pressure is the (radial) force of the

blood against the walls of the arteries.

What is Hypertension?
• The diagnosis of hypertension is based on
repeated, reproducible measurements of
elevated blood pressure
• Essential hypertension (where cause can not be found)
• Non essential hypertension (where cause can be found)

Sustained arterial
hypertension
damages blood
vessels in kidney,
heart, and brain and
leads to an
increased incidence
of renal failure,
coronary disease,
cardiac failure, and
stroke.

BLOOD PRESSURE IN ADULTS:
OLD CLASSIFICATION

BLOOD PRESSURE IN ADULTS:
2017 guidelines

ETIOLOGY
• A specific cause of hypertension can be established in only 10-15%
of patients
• In most cases, elevated blood pressure is associated with an overall
increase in resistance to flow of blood through arterioles, while
cardiac output is usually normal
– Among the known causes of secondary hypertension, kidney disease
ranks first, with tumors or other abnormalities of the adrenal glands
following
• Elevated blood pressure is usually caused by a combination of
several (multifactorial) abnormalities. Epidemiologic evidence points
to genetic inheritance, psychological stress, and environmental and
dietary factors

Risk Factors in Hypertensive Patients

Lack of
Diabetes physical
activity
Chronic
Obesity alcohol
consumption
Family history
Age of CVS
disease
Smoking HYPERTENSION Gender

BASIC PHARMACOLOGY OF
ANTIHYPERTENSIVE AGENTS:
• All antihypertensive
agents act at one or more
of the four anatomic
control and produce their
effects by interfering with
normal mechanisms of
blood pressure regulation.

Basic pathways
involved in the
medullary
control of blood
pressure

Sites of action of the major classes of
antihypertensive drugs
13
 (1) Diuretics, which lower blood pressure by depleting the body of sodium and
reducing blood volume and perhaps by other mechanisms.
 (2) Sympathoplegic agents, which lower blood pressure by reducing

peripheral vascular resistance, inhibiting cardiac function, and increasing
venous pooling in capacitance vessels. (The later two effects reduce cardiac
output.)
 (3) Direct vasodilators, which reduce pressure by relaxing vascular smooth

muscle, thus dilating resistance vessels and to varying degrees increasing
capacitance as well.
 (4) Agents that block production or action of angiotensin and thereby reduce
peripheral vascular resistance and (potentially) blood volume.
 The fact that these drug groups act by different mechanisms permits the
combination of drugs from two or more groups with increased efficacy and, in
some cases, decreased toxicity.

DRUGS THAT ALTER SODIUM
& WATER BALANCE

Mechanisms of Action &
Hemodynamic Effects of Diuretics
 Diuretics lower blood pressure primarily by
depleting body sodium stores
 Diuretics reduce blood pressure by
reducing blood volume and cardiac output;
peripheral vascular resistance may increase
 After 6-8 weeks, cardiac output returns
toward normal while peripheral vascular
resistance declines
 Sodium is believed to contribute to
vascular resistance by increasing vessel
stiffness and neural reactivity. These
effects are reversed by diuretics or sodium
restriction
16
1. Effect blocked by diuretics
2. Effect blocked by ß
blockers

DIURETIC AGENTS
CARBONIC ANHYDRASE INHIBITORS
LOOP DIURETICS
THIAZIDES
POTASSIUM- SPARING DIURETICS
AGENTS THAT ALTER WATER EXCRETION
• Osmotic agents
• ADH Agonists and Antagonists
18
USE OF DIURETICS
• Thiazide diuretics are appropriate for most patients with mild or moderate hypertension
and normal renal and cardiac function
• More powerful diuretics are necessary in severe hypertension, when multiple drugs
with sodium-retaining properties are used; in renal insufficiency, and in cardiac failure or
cirrhosis, where sodium retention is marked
• Potassium-sparing diuretics are useful both to avoid excessive potassium depletion,
particularly in patients taking digitalis, and to enhance the natriuretic effects of other
diuretics
• Aldosterone receptor antagonists in particular also have a favorable effect on cardiac
function in people with heart failure
• Thiazide diuretics lower doses (25-50 mg) exert as much antihypertensive effect as do
higher doses
• In contrast to thiazides, the blood pressure response to loop diuretics continues to
increase at doses many times greater than the usual therapeutic dose

TOXICITY OF DIURETICS
• The most common adverse effect of diuretics (except for potassium-
sparing diuretics) is potassium depletion.
• Although mild degrees of hypokalemia are tolerated well by many
patients, hypokalemia may be hazardous in persons,
– Taking digitalis
– Those who have chronic arrhythmias
– or Those with acute myocardial infarction or left ventricular dysfunction
• Potassium loss is coupled to reabsorption of sodium, and restriction
of dietary sodium intake will therefore minimize potassium loss.
• Diuretics may also cause magnesium depletion, impair glucose
tolerance, and increase serum lipid concentrations.

• Diuretics increase uric acid concentrations and may
precipitate gout.
• Several case-control studies have reported a small but
significant excess risk of renal cell carcinoma associated
with diuretic use.
• Potassium-sparing diuretics may produce hyperkalemia,
particularly in patients with renal insufficiency and those
taking ACE inhibitors or angiotension receptor blockers.
• Spironolactone (a steroid) is associated with
gynecomastia.

DRUGS THAT ALTER SYMPATHETIC
NERVOUS SYSTEM FUNCTION
In patients with moderate to severe hypertension, most

effective drug regimens include an agent that inhibits function
of the sympathetic nervous system.

DRUGS THAT ALTER SYMPATHETIC NERVOUS SYSTEM FUNCTION
CENTRALLY ACTING SYMPATHOPLEGIC DRUGS
GANGLION-BLOCKING AGENTS
ADRENERGIC NEURON-BLOCKING AGENTS
ADRENOCEPTOR ANTAGONISTS

CENTRALLY ACTING
SYMPATHOPLEGIC DRUGS
• These agents reduce sympathetic outflow from vasopressor
centers in the brainstem.
• But allow these centers to retain or even increase their
sensitivity to baroreceptor control.
• Accordingly, the antihypertensive and toxic actions of these
drugs are generally less dependent on posture than are the
effects of drugs that act directly on peripheral sympathetic
neurons.

1. Methyldopa (Aldomet®)
• Methyldopa is an analog of L-dopa and is
converted to α-methyldopamine and α-
methylnorepinephrine; this pathway directly
parallels the synthesis of norepinephrine from
dopa illustrated
• α-Methylnorepinephrine is as potent as
norepinephrine as a vasoconstrictor
• Its substitution for norepinephrine in
peripheral adrenergic neurosecretory vesicles
does not alter the vasoconstrictor response to
peripheral adrenergic neurotransmission
• Rather, α-methylnorepinephrine acts in the
CNS to inhibit adrenergic neuronal outflow
from the brainstem
• USE
– Treatment of mild to moderately severe hypertension
– Most cardiovascular reflexes remain intact after
administration of methyldopa, and blood pressure
reduction is not markedly dependent on maintenance
of upright posture
– Orthostatic hypotension sometimes occurs,
particularly in volume-depleted patients

Pharmacokinetics and Dosage:
• Half life: 2 hrs
• Bioavailability: 25 percent
• Initial Dose: 1 g/d BID or TID
• Usual Maintenance dose: 1-2 g/d BID or TID
• IV 250–500 mg q6h
• Does not reqiure adjustment in renal compromised
patients

Toxicity
• Sedation
• Lassitude
• Nightmares
• Lactation (with increased prolactin secretion
due to inhibition of dopaminergic neuron in
hypothalamus)

2. Clonidine (Catapres ®)
• Clonidine reduces sympathetic and increases
parasympathetic tone, resulting in blood pressure
lowering and bradycardia
• The alpha2-agonistic activity contributes to its BP-
lowering effect due to negative feedback at the
presynaptic neurons
• Blood pressure lowering by clonidine results from,
– Reduction of cardiac output due to decreased heart
rate
– Relaxation of capacitance vessels, with a reduction in
peripheral vascular resistance
Pharmacokinetics & Dosage
• Half life: 8-12 hrs
• Initial Dose: 0.2 mg/d q12h
• Usual Maintenance dose: 0.2-1.2 mg/d q8h
• Does reqiure adjustment in renal compromised patients.
• A transdermal preparation of clonidine that reduces blood
pressure for 7 days after a single application is also
available.
*Clonidine supression test

Toxicity
• Dry mouth and sedation are frequent and may be
severe
• The drug should not be given to patients who are
at risk for mental depression and should be
withdrawn if depression occurs during therapy
• Clonidine also causes Na+ and H2O retention
• Abrupt withdrawal may induce hypertensive crisis
3. Guanabenz and guanfacine
• Similar to clonidine in action
• centrally active antihypertensive drugs that
share the central alpha-adrenoceptor-
stimulating effects of clonidine

GANGLION-BLOCKING
AGENTS
(e.g. Trimethaphan)
• Ganglion blockers competitively block

nicotinic cholinoceptors on postganglionic
neurons in both sympathetic and
parasympathetic ganglia.

Adverse effects
• The adverse effects of ganglion blockers are
direct extensions of their pharmacologic effects.
These effects include both
– Sympathoplegia (excessive orthostatic hypotension

and sexual dysfunction)
and
– Parasympathoplegia (constipation, urinary retention,
precipitation of glaucoma, blurred vision, dry mouth,
etc).
ADRENERGIC NEURON-
BLOCKING AGENTS
These drugs lower blood pressure by

preventing normal physiologic release of
norepinephrine from postganglionic
sympathetic neurons.

GUANETHIDINE (Ismelin®)
• In high enough doses, guanethidine can produce
profound sympathoplegia.
• For the same reason, guanethidine can produce
all of the toxicities expected from "pharmacologic
sympathectomy", including marked postural
hypotension, diarrhea, and impaired ejaculation.
Because of these adverse effects, guanethidine is
now rarely used.

Mechanism & Sites of Action
• Guanethidine inhibits the release of
norepinephrine from sympathetic
nerve endings.
• Once guanethidine has entered the
nerve, it is concentrated in
transmitter vesicles, where it
replaces norepinephrine. Because it
replaces norepinephrine, the drug
causes a gradual depletion of
norepinephrine stores in the nerve
ending.

• Half life: 5 days
• Bioavailability: 3 - 50 percent
• Initial Dose: 10 mg/d PO
• Usual Maintenance dose: 25 - 50 mg/d PO

Toxicity
• Symptomatic postural hypotension and
hypotension following exercise, particularly
when the drug is given in high doses, and may
produce dangerously decreased blood flow to
heart and brain or even overt shock
• Diarrhea

RESERPINE
• Reserpine, an alkaloid extracted from the
roots of an Indian plant, Rauwolfia serpentina,
was one of the first effective drugs used on a
large scale in the treatment of hypertension.

• Reserpine blocks the
ability of aminergic
transmitter vesicles to
take up and store
biogenic amines,
probably by interfering
with the vesicular
membrane-associated
transporter
41
• Half life: 24-48 hrs
• Initial Dose: 0.25 mg/d
• Usual Maintenance dose: 0.25 mg/d
• Does not reqiure adjustment in moderately renal
compromised patients.

Toxicity
• Enters into brain easily and can produce sedation,
mental depression, Parkinson’s like symptoms.
• Should not be given to patients with mental
depression or peptic ulcer (for its GI-stimulating
effect).
• Drowsiness, sedation, lethargy, respiratory
depression, edema, orthostatic hypotension and
nasal congestion.
ADRENOCEPTOR
ANTAGONISTS
Beta Alpha
blockers blockers

β-blockers.
• Propranolol, metoprolol, nadolol, carteolol, atenolol,
betaxolol, bisoprolol,pindolol, acebutolol, penbutolol,
labetalol, carvedilol.

PROPRANOLOL (Inderal®)
• Propranolol was the first beta blocker shown to
be effective in hypertension and ischemic heart
disease.
• Useful for lowering blood pressure in mild to
moderate hypertension.
• In severe hypertension, beta blockers are
especially useful in preventing the reflex
tachycardia that often results from treatment
with direct vasodilators.
• Propranolol decreases blood pressure
primarily as a result of a decrease in cardiac
output.
• Propranolol inhibits the stimulation of renin
production by catecholamines (mediated by
beta1 receptors).

• Half life: 3-5 days
• Initial Dose: 80 mg/d PO
• Usual Maintenance dose: 80-480 mg/d PO
• Does not require dose adjustment in moderate renal
insufficiency.
• Administered once or twice daily.

Toxicity
• Rash, fever, and other manifestations of drug
allergy are rare
• Sedation, sleep disturbances, and depression.
Rarely, psychotic reactions may occur
• Worsening of pre-existing asthma and other
forms of airway obstruction

OTHER BETA-ADRENOCEPTOR-BLOCKING AGENTS
• Metoprolol
– Less potent than propranolol in blocking beta2 receptors
• Nadolol, Carteolol
– Nadolol and carteolol, nonselective beta-receptor
antagonists
• Atenolol
– Beta1-selective blocker
• Betaxolol and bisoprolol
– Beta1-selective blockers that are primarily metabolized in
the liver but have long half-lives
• Pindolol, Acebutolol, & Penbutolol
– Partial agonists, i.e. β blockers with some intrinsic sympathomimetic activity
• Labetalol
– Is formulated as a racemic mixture of four isomers
– The (S,S)- and (R,S)-isomers are relatively inactive, a third (S,R)- is a potent alpha
blocker, and the last (R,R)- is a potent beta blocker
– The β-blocking isomer is thought to have selective β 2 agonist and nonselective β
antagonist action
• Carvedilol
– Administered as a racemic mixture
– The S(-) isomer is a nonselective beta-adrenoceptor blocker, but both S(-) and R(+)
isomers have approximately equal alpha-blocking potency
• Esmolol
– Beta1-selective blocker that is rapidly metabolized via hydrolysis by red blood cell
esterases
– It has a short half-life (9-10 minutes) and is administered by constant intravenous
infusion

α1-blockers.
• Prazosin, terazosin, doxazosin, phentolamine,
phenoxybenzamine

• Prazosin, terazosin and doxazosin produce most of

their antihypertensive effect by selectively blocking
alpha1 receptors in arterioles and venules
• Phentolamine is antagonist for both α1 and α2
• Phenoxybenzamine is an irreversible blocker for α1 and

α2

• Phenoxybenzamine binds covalently to α receptors,
causing irreversible blockade of long duration
– Absorbed after oral administration, although bioavailability
is low
– Usually given orally, starting with dosages of 10 mg/d and
progressively increasing the dose until the desired effect is
achieved
– The most important ADRs include orthostatic hypotension
and tachycardia,
• Nasal stuffiness and inhibition of ejaculation also occur
• Since phenoxybenzamine enters the CNS, it may cause less specific effects including
fatigue, sedation, and nausea

• Phentolamine is a potent competitive antagonist at
both α1 and α2 receptors
– Phentolamine reduces peripheral resistance through
blockade of α1 receptors and possibly α2 receptors on
vascular smooth muscle
– Its cardiac stimulation is due to antagonism of presynaptic
α2 receptors

Prazosin (Minipress®)
• Half life: 3-4 days

• Initial Dose: 3 mg/d PO 12h
• Usual Maintenance dose: 10-30 mg/d PO 24h
• Does not require dose adjustment in moderate renal
insufficiency
VASODILATORS

• Within this class of drugs are,
1. The oral vasodilators, hydralazine and minoxidil, which

are used for long-term outpatient therapy of
hypertension;
2. The parenteral vasodilators, nitroprusside, diazoxide,

and fenoldopam, which are used to treat hypertensive
emergencies; and
3. The calcium channel blockers, which are used in both

circumstances.

HYDRALAZINE
A hydrazine derivative, dilates arterioles but not veins
Works by causing release of NO
• Well absorbed and rapidly metabolized by the liver during the first pass, so
that bioavailability is low
• The half-life of hydralazine ranges from 1.5 to 3 hours, but vascular effects
persist longer than do blood concentrations (why?)
Toxicity
• headache, nausea, anorexia, palpitations, sweating, and flushing
• In patients with ischemic heart disease, reflex tachycardia and
sympathetic stimulation may provoke angina or ischemic arrhythmias

MINOXIDIL (Minoxin ®)
• Minoxidil is a very efficacious orally active vasodilator
• The effect results from the opening of potassium channels in smooth muscle
membranes by minoxidil sulfate, the active metabolite. Increased potassium
permeability stabilizes the membrane at its resting potential and makes contraction less
likely
• Like hydralazine, minoxidil dilates arterioles but not veins
• 5 to 100 mg 24 hourly PO
Toxicity
• Tachycardia, palpitations, angina, and edema are
observed, Headache, sweating, and hirsutism

SODIUM NITROPRUSSIDE
• A powerful parenterally administered vasodilator
• Nitroprusside dilates both arterial and venous vessels
• The action occurs as a result of activation of guanylyl cyclase. The result is
increased intracellular cGMP, which relaxes vascular smooth muscle
• It is rapidly metabolized by uptake into red blood cells with liberation of
cyanide
• Nitroprusside rapidly lowers blood pressure, and its effects disappear within 1-
10 minutes after discontinuation
• Dosage typically begins at 0.5 mcg/kg/min and may be increased up to 10
mcg/kg/min as necessary to control blood pressure
Toxicity
• Excessive blood pressure lowering
• Accumulation of cyanide; metabolic acidosis, arrhythmias, excessive
hypotension, and death

DIAZOXIDE
• Diazoxide is an effective and relatively long-acting parenterally
administered arteriolar dilator
• Diazoxide is partially metabolized. The remainder is excreted
unchanged
• Its half-life is approximately 24 hours
Toxicity
• Excessive hypotension, the reflex sympathetic response can
provoke angina and cardiac failure in patients with ischemic heart
disease, and diazoxide should be avoided in this situation

FENOLDOPAM
• Fenoldopam is a peripheral arteriolar dilator
used for hypertensive emergencies and
postoperative hypertension
• It acts primarily as an agonist of dopamine D1
receptors, resulting in dilation of peripheral
arteries and natriuresis

1. Effect blocked by diuretics
2. Effect blocked by ß
blockers

CALCIUM CHANNEL BLOCKERS
• The mechanism of action in
hypertension is inhibition of calcium
influx into arterial smooth muscle cells.
• Verapamil
• Diltiazem, and the
• Dihydropyridine family
– Amlodipine,
– Felodipine,
– Isradipine,
– Nicardipine,
– Nifedipine, and
– Nisoldipine
• are all equally effective in lowering
blood pressure.

Pharmacokinetics
• The calcium channel blockers are orally active
agents and are characterized by high first-pass
effect, high plasma protein binding, and
extensive metabolism
• Verapamil and diltiazem are also used by the
intravenous route

Toxicity
• Excessive inhibition of calcium influx can cause
serious cardiac depression, including cardiac
arrest, bradycardia, atrioventricular block, and
heart failure
• These effects have been rare in clinical use

Agents that block production or
action of angiotensin
• ACE INHIBITORS.
• ARBs
• DRIs.

ANGIOTENSIN-CONVERTING
ENZYME (ACE) INHIBITORS
• Drugs in this class inhibit the converting enzyme
peptidyl dipeptidase that hydrolyzes angiotensin I to
angiotensin II and (under the name plasma kininase)
inactivates bradykinin

Examples:
• Captopril (Capoten®)
• Enalapril (Renitec®)
– is an oral prodrug that is converted by hydrolysis to a converting enzyme
inhibitor, enalaprilat, with effects similar to those of captopril.
• Lisinopril (zestril®)
– is a lysine derivative of enalaprilat.
• Long-acting members of the class (which are all prodrugs) include,

– Benazepril, fosinopril, moexipril, perindopril, quinapril, ramipril, and
trandolapril

– Peak concentrations of enalaprilat, occur 3-4 hours after dosing with enalapril
– All of the ACE inhibitors except fosinopril and moexipril are eliminated
primarily by the kidneys
Toxicity
– Severe hypotension can occur after initial doses of any ACE inhibitor in
patients who are hypovolemic due to diuretics, salt restriction, or
gastrointestinal fluid loss
– Acute renal failure, hyperkalemia, dry cough sometimes accompanied by
wheezing, and angioedema
– ACE inhibitors are contraindicated during the second and third trimesters of
pregnancy because of the risk of fetal hypotension, anuria, and renal failure,
sometimes associated with fetal malformations or death

ANGIOTENSIN RECEPTOR-BLOCKING
AGENTS
• Losartan and valsartan were the first marketed.
• candesartan, eprosartan, irbesartan, and
telmisartan are newer…
• NO EFFECT on bradykinin metabolism
• More Selective blockers of angiotensin effects than
ACE inhibitors

Renin Inhibitors
• In patients with essential hypertension, aliskiren
suppresses plasma renin activity and causes dose-
related reductions in blood pressure similar to those
produced by angiotensin II receptor antagonists
• Aliskiren (Rasilez®)
– Aliskiren binds to the binding pocket of Renin, essential
for its activity
– Binding to this pocket prevents the conversion of
angiotensinogen to angiotensin I
THERAPEUTICS
• Hypertension is a life long disease and its teatment has potential to pose burden
on Pocket and Safety of Patients
• Persistency of Hypertension should be established with certainty
– Readings for at least 3 different visits should be considered
– Assessment of blood pressure should include measurement of recumbent, sitting, and
standing pressures
• Secondary causes must be excluded
• Drug treatment should be established considering,
• The level of blood pressure
• The age of the patient
• The severity of organ damage (if any)
• The presence of cardiovascular risk factors
• Assessment of renal function and the presence of proteinuria are useful in antihypertensive
drug selection
• Failure of treatment might be due to,
– Noncompliance with medication
– Excessive sodium intake
– Inadequate diuretic therapy
– Drugs such as,
• Tricyclic antidepressants
• Nonsteroidal anti-inflammatory drugs
• Over-the-counter sympathomimetics
– Amphetamine or cocaine etc
• Excessive doses of caffeine and oral contraceptives

How do I control my high blood pressure?
Answer to the question from FDA
• Check your blood pressure regularly
• Take your high blood pressure medicine every day if needed
• Exercise often
• Eat foods low in salt
• Lose weight or keep weight at a healthy level
• Do not smoke
• Limit alcohol
• Talk to your doctor regularly about your pressure

JNC 7 GUIDELINES

JNC 8 GUIDELINES (PUBLISHED 2014)

2017 GUIDELINES
(SEPARATELY PROVIDED AS SUPPLEMENTARY MATERIAL)

Look into the guidelines separately provided
and answer following questions
• When were the first comprehensive guidelines regarding hypertension and
its management published?
• Mention categories of blood pressure values in adults.
• While taking blood pressure measurements patient should be at rest;
What are the specific instructions that you can apply to ensure this?
• Which arm of the patient, left or right, should we use to take blood
pressure measurements?
• What is white coat hypertension?
• What is masked hypertension?
• What is resistant hypertension?
88
• What are the five most common secondary causes of hypertension?
• In overweight individuals, how much ecrease in SBP can you expect with
every kg drop in body weight?
• What should be the treatment strategy in stage I hypertension with no co-
morbidities and less than 10% CVD risk in 10 years?
• Draw flow charts for the treatment of hypertension with following co-
morbidities,
– Stable ischemic heart disease
– Chronic kidney disease
• Enumerate primary antihypertensive agents given by oral route.

Hypertensive Emergencies
• Oral antihypertensive:
– (captopril, clonidine, or labetolol).
• Intravenous medication.
– Sodium nitroprusside, Nicardipine hydrochloride,
Fenoldopam mesylate, Nitroglycerin, Enalaprilat,
Hydralazine hydrochloride, Labetalol
hydrochloride, Esmolol hydrochloride.


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PHARMACOLOGY & THERAPEUTICS –II

Dr. Auwais Ahmed Khan

Dr. Auwais Ahmed Khan 2

• Blood pressure is the (radial) force of the

Dr. Auwais Ahmed Khan 3

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Smoking HYPERTENSION Gender

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 (2) Sympathoplegic agents, which lower blood pressure by reducing

 (3) Direct vasodilators, which reduce pressure by relaxing vascular smooth

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CARBONIC ANHYDRASE INHIBITORS

POTASSIUM- SPARING DIURETICS

AGENTS THAT ALTER WATER EXCRETION

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In patients with moderate to severe hypertension, most

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CENTRALLY ACTING SYMPATHOPLEGIC DRUGS

ADRENERGIC NEURON-BLOCKING AGENTS

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• Ganglion blockers competitively block

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– Sympathoplegia (excessive orthostatic hypotension

These drugs lower blood pressure by

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• Prazosin, terazosin and doxazosin produce most of

• Phentolamine is antagonist for both α1 and α2

• Phenoxybenzamine is an irreversible blocker for α1 and

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• Half life: 3-4 days

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