Nifedipine is a calcium-channel antagonist having the property of selective inhibition of transmembrane flux of calcium in excitable tissues.¹ Its ability to block calcium-mediated electromechanical coupling in contractile tissue produces arterial dilation in both the coronary and peripheral vascular beds and provides the clinical rationale for use of the drug in the management of myocardial ischemic syndromes. Because systemic vasodilation can be expected to reduce elevated arterial BP, interest has focused on the use of nifedipine in the medical management of systemic hypertension. A postulated involvement of calcium in the development of the increased vascular tone of hypertension, makes nifedipine, and the other calcium-channel antagonists, appear particularly attractive for use as vasodilators.²

See also p 2357.

The effectiveness of nifedipine in the acute treatment of severe hypertension and hypertensive emergencies has been demonstrated in several studies,^3-6 including the study by Haft and Litterer³ in this Archives