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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)