ANTI-HYPERTENSIVE DRUGS MODE/MECHANISM OF ACTION

 ANGIOTENSIN II RECEPTOR BLOCKERS

 TELMISARTAN Blocks the vasoconstrictive and aldosterone-secreting effects

of angiotensin II by selectively blocking the binding of
angiotensin II to the ATI receptor in many tissues (vascular
smooth muscles and adrenal gland).
 LOSARTAN Selectively blocks the binding of angiotensin II to receptor
sites in many tissues, especially the vascular smooth muscles
and adrenal glands. This prevents the vasoconstricting and
aldosterone-secreting effects of angiotensin II on these
tissues.
 VALSARTAN Blocks the vasoconstrictor and aldosterone-secreting effects
of angiotensin II; selectively blocks the binding of
angiotensin II to the ATI receptor found in tissues.

 ACE INHIBITORS

 CAPTOPRIL Selectively suppresses renin angiotensin-aldosterone system;

inhibits ACE; prevents conversion of angiotensin I to
angiotensin II.
 LISINOPRIL It prevents the conversion of angiotensin I to angiotensin II, a
potent vasoconstrictor. This results to vasodilation and
decreased peripheral resistance and suppression of the renin-
angiotensin-aldosterone system.

 SYMPATHOLYTICS
A. ALPHA 1 RECEPTOR BLOCKERS

 PRAZOSIN Prazosin inhibits the postsynaptic alpha-1

adrenoceptors. This inhibition blocks the
vasoconstricting (narrowing) effect of
catecholamines (epinephrine and norepinephrine)
on the vessels, leading to peripheral blood vessel
dilation. Through blood vessel constriction by
adrenergic receptor activation, epinephrine and
norepinephrine normally act to increase blood
pressure
 TERAZOSIN Alpha 1 – adrenergic receptor antagonist. It
 decreases blood pressure through vasodilation in
response to Alpha 1 – adrenergic receptor blockade.
It also improves urine flow by relaxation of the
smooth muscles of the bladder neck and prostate to
relieve urethral pressure.

B. ALPHA 2 AGONIST

 METHYLDOPA The active metabolite alpha-methyl

norepinephrine stimulates central alpha 2
adrenergic receptors in the CNS, resulting in
decreased sympathetic outflow from the brain to
the heart, kidneys and peripheral vasculature.
 CLONIDINE Stimulates central alpha-adrenergic receptors to
inhibit sympathetic cardio accelerator and
vasoconstrictor centers.

C. BETA BLOCKERS

 METOPROLOL Exerts mainly Beta 1 adrenergic blocking activity

but also blocks Beta 2 receptors at high doses. It
reversibly and competitively combines with Beta
1 adrenergic receptors to block sympathetic
nerve impulses, resulting to decreased myocardial
contractility, heart rate, cardiac output and
myocardial oxygen consumption. These effects
lead to decreased blood pressure and reversal of
cardiac arrhythmias, consequently preventing
myocardial tissue damage.

D. ALPHA 1 AND BETA 1 BLOCKER

 LABETALOL Labetalol non-selectively antagonizes beta-

adrenergic receptors, and selectively antagonizes
alpha-1-adrenergic receptors. Antagonism of alpha-
1-adrenergic receptors leads to vasodilation and
decreased vascular resistance.This leads to a
decrease in blood pressure that is most pronounced
while standing. Labetalol leads to sustained
vasodilation over the long term without a significant
 decrease in cardiac output or stroke volume, and a
minimal decrease in heart rate.

E. DIRECT ACTING ARTERIAL VASODILATORS

 HYDRALAZINE Directly relaxes arteriolar smooth muscles to

cause vasodilation and decreased blood pressure.

 CALCIUM CHANNEL BLOCKERS

 AMLODIPINE Inhibits influx of calcium ion across cell membranes to

produce relaxation of coronary vascular smooth muscle
(dilatation of coronary arteries), decrease peripheral vascular
resistance of smooth muscle (decrease blood pressure) and
increases myocardial oxygen delivery in patient with
vasospastic angina.
 NICARDIPINE Inhibits calcium ion influx across cell membrane during
cardiac depolarization, produces relaxation of coronary
vascular smooth muscle and peripheral vascular smooth
muscle, dilates coronary arteries, and increases myocardial
oxygen delivery in patients with vasospastic angina.
 FELODIPINE Inhibits calcium ion influx across cell membrane, resulting in
inhibition of excitation/contraction.
 NIFEDIPINE Inhibits calcium ion influx across cell membrane during
cardiac depolarization, produces relaxation of coronary
vascular smooth muscle and peripheral vascular smooth
muscle, dilates coronary vascular arteries, increases
myocardial oxygen delivery in patients with vasospastic
angina.