Use of nifedipine in hypertension and Raynaud's phenomenon

Abstract

The reduction of transmembranous calcium influx into vascular smooth muscle cells by calcium antagonists leads to a reduction of tension development and vascular tone. Nifedipine reduces forearm vascular resistance dose-dependently when infused into the brachial artery in patients with essential hypertension, attesting to its potent arterial vasodilator effects. This effect can be successfully utilized for the treatment of essential hypertension, where nifedipine acts by reducing increased peripheral vascular resistance, thereby normalizing the main hemodynamic derangement of hypertensive patients. In contrast to other direct-acting vasodilators, the antihypertensive effect is not accompanied by sympathetic reflex activation or volume retention, making it feasible to use nifedipine as monotherapy for hypertensive patients. Although the pathophysiologic disturbances leading to vasospasm are not clear, blockade of slow calcium channels is also effective for the treatment of Raynaud's phenomenon, reducing attack frequency, digital pain, and functional disability in many patients, particularly those with primary Raynaud's phenomenon.