Acute arteriolar vasoconstriction is considered to be the common physiologic pathway for hypertensive crises. Calcium plays a critical role in this process as a required element in the generation of vascular smooth muscle contraction. Within the vascular smooth muscle cell, calcium homeostasis is maintained through a complex set of mechanisms that control cellular calcium influx and efflux as well as intracellular calcium storage. Extracellular calcium enters the intracellular free space of the vascular smooth muscle cell through four portals: a passive slow leak, voltage-gated channels, hormone-mediated receptor-operated channels, and stretch-activated channels. The myofilaments actin and myosin contract upon the increase in cytosolic calcium. Calcium-channel blockers are commonly used as vasodilators for the treatment of hypertensive crises. There are three families of commercially available calcium-channel blockers: 1,4 dihydropyridines, phenylalkylamines, and benzothiazepines. These drugs block extracellular calcium entry through the L-type voltage-gated channel. Systemic vasodilation is produced as the cytosolic calcium level is lowered and myosin-actin contraction cannot be maintained. The precise mechanism of blockade and the tissue site selectivity varies among the three drug families. The 1,4 dihydropyridines are selective for the arteriolar beds, while the phenylalkylamines and benzothiazepines are selective for the atrioventricular node. Of the calcium-channel blockers, the dihydropyridines nifedipine and nicardipine are recommended as first-line agents for hypertensive emergencies and urgencies because of their peripheral arteriolar bed selectivity and their pharmacologic and kinetic profiles.