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Table 1 Pharmacological rationale of combination therapy

From: Combination therapy in hypertension: An update

Combinations

Mechanisms

ARB-Diuretic

ARBs cause the antagonism of angiotensin II at the vascular and myocardial level by direct AT-1 receptor blockade

Thiazide diuretic blocks sodium chloride reabsorption at the distal convoluted tubule

β-Adrenoceptor Antagonist-Diuretic

The β-adrenoceptor blocker inhibits activation by direct suppression of renin release, inhibit β-adrenergic sympathetic stimulation decreasing myocardial contractility and heart rate

Diuretics as above

ACEI-Diuretic

ACEI cause the removal of the angiotensin II effect (vasoconstriction, stimulation of aldosterone secretion) and enhancement of kinin-mediated vasodilation

Diuretics as above

ACEI-CCB

ACEI as above

The calcium antagonists de-crease vascular resistance by vascular smooth muscle relaxation

ARB-CCB

ARBs as above

CCBs as Above

ACE-ARB Inhibitors

ACEI as above

ARBs as above

Centrally Acting Agents-Diuretic

Clonidine acts by decreasing sympathetic outflow by stimulating pre synaptic α2-adrenoceptors in the vasomotor centre of the CNS.

Diuretics as above

  1. Angiotensin Converting Enzyme (ACE) inhibitors, Angiotensin II type 1 Receptor Blockers (ARBs), Calcium Channel Antagonist (CCB)