The most commonly used clinical antihypertensive drugs are now in five categories: first, diuretics. The antihypertensive effect is mainly through sodium excretion, reducing extracellular volume and lowering peripheral vascular resistance, thus exerting a hypotensive effect. The second, beta-blockers. The antihypertensive effect is through the inhibition of the central and peripheral RAAS system, that is, the renin-angiotensin-aldosterone system, thus inhibiting myocardial contractility and slowing down the heart rate, and exerting the antihypertensive effect. The third, calcium channel blockers. The antihypertensive effect is mainly through blocking voltage-dependent L-type calcium channels and reducing the entry of extracellular Ca+2 into vascular smooth muscle. Simply put, inhibiting Ca+2 inward flow, thereby attenuating excitation-contraction coupling, reduces the contractile response of resistance vessels. In addition, calcium channel blockers attenuate the constrictive effects of AT II and α1-adrenergic receptors and reduce sodium reabsorption by the renal tubules. The fourth, angiotensin-converting enzyme inhibitor, or ACEI, reduces ATII production by inhibiting ACE, or angiotensin-converting enzyme, in circulation and tissues, and reduces bradykinin degradation by inhibiting bradykininase, which increases bradykinin to exert antihypertensive effects. The fifth, angiotensin II receptor antagonist, abbreviated as ARB, exerts its antihypertensive effect mainly by blocking the tissue ATII receptor subtype AT1, which more fully and effectively blocks the vasoconstriction and water and sodium retention effects of ATII.