To summarize, ACE inhibitors are considered second-line therapy to diuretics in most patients with hypertension. ACE inhibitors competitively inhibit ACE enzymes, mimicking the structure of its substrate and thereby block the conversion of angiotensin I to angiotensin II. Inhibition of Angiotensin II formation (which acts at AT-1 receptors and stimulating vasoconstriction and aldosterone release) will reduce both the vasoconstrictor and Na+ retention effects of the RAAS, explaining their antihypertensive action. The angiotensin receptor blockers (ARB) binding to type I angiotensin II receptors (AT1) and thereby antagonize or block the effects of angiotensin II type 1 receptor mediated effects of Ang II. This effect is more specific on AT-II action, and less or none on bradykinin production or metabolism. Calcium channel blockers are not first-line agents but are very effective antihypertensive agents, especially in African-American patients. Calcium channel blockers bind to L-type calcium channels and reduce calcium influx. This can have its effect at three locations: (1) the conducting system of the heart—the drugs slow the conductance of cardiac excitation, (2) the contractile cardiac myocytes—the drugs reduce the force of contraction and (3) the vascular smooth muscle cells—the drugs vasodilate, seen in a wide manner across arterial beds. This is predominantly on the arterial side, including the resistance precapillary arterioles, leading to a reduction in peripheral resistance which in turn reduce blood pressure.

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