Vasoconstriction results from an exaggerated increase of intracellular Ca2+ concentration which initiates the contractile process within the vascular smooth muscle. The dependency of these cells on extracellular Ca2+ to trigger the contractile process when exposed to naturally occurring vasoactive substances such as those released from aggregating blood platelets varies in different vascular areas. This is one of the factors that determine the different sensitivity to the inhibitory effect of various calcium antagonist. A blood vessel can be more reactive to some calcium antagonists than to others, depending on the vascular area. Experiments on isolated cerebral arteries suggest that inhibition of cerebral vasoconstriction is observed with substances such as flunarizine under conditions of vascular hyperresponsiveness generated by acute or chronic pathological conditions or triggered by interaction between vasoactive substances. In this regard marked differences exist between the individual calcium antagonists. Those that are selective for slow Ca2+ channels will inhibit myocardial contractile force and decrease vascular myogenic activity (e.g., at the arteriolar level). Such inhibitory activity is not observed with flunarizine, which affects Ca2+ entry rather selectively, when calcium overload is imposed upon the vasculature, in particular at cerebrovascular sites. This suggests a potential use of this compound in a number of neurological disorders related to cerebral ischemia.