Abstract
Abnormal narrowing of the arterioles, caused by contraction of arteriolar smooth muscle, contributes to the genesis and the maintenance of the increased peripheral resistance observed in hypertension. Activation of the contractile process in vascular smooth muscle requires an increase in cytoplasmic calcium. In most blood vessels, the activator ion enters the cell through specific membrane channels, which can be inhibited by a chemically heterogeneous group of drugs, the calcium-entry blockers. The antihypertensive effect of these agents is probably explained by their inhibitory effect on (1) α-adrenergic activation (the pharmacologic subtype of postjunctional α-adrenoceptor does not necessarily determine the importance of calcium entry); (2) activation by nonadrenergic neurohumoral mediators (for example, serotonin); (3) acceleration of calcium entry by metabolites of arachidonic acid formed by lipoxygenase; and (4) inherent myogenic tone.
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