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.