Antihypertensive effect of a calcium antagonistic drug: Regression of hypertensive cardiac hypertrophy by nifedipine

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Abstract
The cardiac hypertrophy which develops in models of sustained hypertension in experimental animals cannot be prevented or reversed by all antihypertensive drugs. Clearly, blood pressure is only one of numerous factors which contribute to the development of hypertensive cardiomegaly. The ability of drugs to reduce cardiac hypertrophy depends primarily on their mode of action, rather than on the degree of blood pressure decrease. Vasodilators effectively control high blood pressure but enhance cardiac hypertrophy in rats. In currect experiments, minoxidil lowered blood pressure, but caused increases in heart weight and plasma‐renin activity (PRA) in spontaneously hypertensive rats (SHR). In contrast, the calcium antagonist, nifedipine, reduced blood pressure or prevented its increase in SHR concurrently reducing heart wight and decreasing PRA. Moreever, nifedipine prevented salt‐induced hypertension and heart hypertrophy in SD (sensitive)‐Dahl rats. It is suggested that in contrast to the vasodilator minoxidil, nifedipine reduces the high renovascular resistance in hypertensives thus enhancing sodium and water elimination. Thus, the action of the calcium antagonist, nifedipine, involve both renal vasodilation and reduction of renin‐angiotensin mediated renal vasoconstriction. In this way, the decreased volume load together with the decreased arterial afterload will contribute to the prevention or regression of hypertensive cardiac hypertrophy.