Vascular aspects of calcium antagonists

Calcium antagonistic drugs have been recognized as useful antiarrhythmic agents for approximately a decade. More recently, however, their vascular effects have been shown to be of potential therapeutic and pharmacological interest, especially in the treatment of angina pectoris involving coronary arterial spasm and possibly also of hypertension. The present survey is dealing with the circulatory changes of the calcium antagonists, describing the influence of the drugs on the systemic and coronary circulation, as well as on special vascular beds like the renal and cerebral circulatory tracts. The influence of the calcium antagonistic agents on vascular smooth muscle at a cellular level is the main subject of the present article. The calcium antagonists inhibit the influx of calcium ions into the cell. Accordingly, they prevent the vasoconstriction, induced by the stimulation of vascular alpha 2-adrenoceptors. However, the calcium antagonists do not block alpha 2-adrenoceptors as such, but they prevent the stimulation of the contractile proteins. This type of interaction has been demonstrated in various animal species for a variety of calcium antagonists on the one hand and for several selective or non-selective alpha 2-adrenoceptor stimulants on the other hand. The vasodilator effect of calcium antagonists may be explained by the selective inhibition of the vasoconstriction, induced by the stimulation of alpha 2-adrenoceptors by endogenous (nor)adrenaline.