Abstract
The therapeutic efficacy of calcium antagonists in ischemic disorders of various tissues is attributed to vasodilator and antivasoconstrictor activities. A direct, energy-conserving, antiischemic effect of certain calcium antagonists has been claimed repeatedly by basic scientists. The clinical value of such effects has been doubtful until recently, when the organ-protective activity of certain calcium antagonists was confirmed in a few large-controlled clinical trials. The following evidence has been presented for the protective activity of calcium antagonists: (1) for the heart, beneficial effects of verapamil and diltiazem have been shown on reinfarction and mortality rates, (2) relative to the brain, the beneficial effect of nimodipine has been shown in preventing neurologic deficits after subarachnoidal hemorrhage, and an antimigraine effect of flunarizine has been demonstrated, (3) concerning the blood vessels, israpidine and lacidipine have been demonstrated to have antiatherogenic potency in animal models, and (4) for the kidneys, an antivasoconstrictor effect occurs at the preglomerular level. In addition, verapamil, diltiazem, and nitrendipine may protect against radiocontrast-induced nephrotoxicity, and verapamil counteracts cyclosporine nephrotoxicity.
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