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Abstract
Calcium channel blocking drugs (CCB) have been used to lower blood pressure since 1970. Three classes are currently available, the phenylalkylamines, the benzothiazepines, and the dihydropyridines. The structure of the L-type, voltage dependent calcium channel has been elucidated with molecular techniques and the different binding sites of the various CCB described. CCB have specific effects at the site of target organs. In the kidney, all classes produce natriuresis. Their action appears independent of the level of salt intake. CCB may favorably influence the course of chronic renal disease; the results of a trial comparing nifedipine to the converting enzyme inhibitor captopril showed no difference between the two drugs. CCB may impede the progression of atherosclerosis in the coronary arteries; a prospective study of nifedipine on coronary artery morphology supports this view. In the brain, nimodipine improves the outcome of patients with stroke from subarachnoid hemorrhage. Positive effects on patients with ischemic stroke have not been corroborated. CCB are approved primary treatment for patients with hypertension and are readily combined with other antihypertensive agents. They are well tolerated and have no adverse metabolic side effects. The advent of molecular pharmacology will advance current efforts to develop new CCB, which are highly selective in their site and mode of action.