**1. Introduction**

Vasospasm is a condition which is associated with an arterial spasm and vasoconstriction, which may lead to tissue ischemia and necrosis. Coronary vasospasm can lead to significant cardiac ischemia associated with symptomatic ischemia or cardiac arrhythmia. Cerebral vasospasm may arise as a complication of subarachnoid hemorrhage (SAH). The most common cause of delayed cerebral ischemia after SAH is assumed to be vasospasm; delayed cerebral ischemia contributes substantially to morbidity and mortality after SAH especially aneurysmal SAH. Calcium channel blockers are widely used in the treatment of hypertension, angina pectoris, cardiac arrhythmias, and other disorders like SAH vasospasm related and migraine. Data is suggesting that their use reduces the risk of subsequent cardiovascular events [1, 2]. Besides, some meta-analyses have suggested that calcium channel blockers may be more effective than other drugs in reducing stroke risk [3, 4]. Fleckenstein's work in the 1960s led to the concept that drugs alter cardiac and smooth muscle contraction by blocking the entry of Ca2+ into myocytes. Godfraind and associates showed that the effect of the diphenylpiperazine analogs in the prevention of agonist-induced vascular smooth muscle contraction could be overcome by raising the concentration

of Ca2+ in the extracellular medium. Hass and Hartfelder reported in 1962 that verapamil, a coronary vasodilator, possessed negative inotropic and chronotropic effects that were not seen with other vasodilatory agents, such as GTN. In 1967, Fleckenstein suggested that the negative inotropic effect resulted from an inhibition of excitation-contraction coupling and that the mechanism involved reduced movement of Ca2+ into cardiac myocytes. Verapamil was the first clinically available Ca2+ channel blocker; it is a congener of papaverine. Many other Ca2+ entry blockers with a wide range of structures are now available [5].
