van Zwieten P A, Timmermans P B, Thoolen M J, Wilffert B, De Jonge A
Am J Cardiol. 1986 Feb 26;57(7):11D-15D. doi: 10.1016/0002-9149(86)90799-x.
A survey is given of the mechanisms of the antihypertensive effect of calcium entry blockers. The main background of the antihypertensive/hypotensive action is dilatation of precapillary arterioles (resistance vessels that cause a reduction in total peripheral resistance and, hence, a decrease in blood pressure). The vascular relaxation is caused by an inhibition of the transmembranous calcium influx and, probably less so, by interference with calmoduline. Calcium entry blockers significantly reduce the vasoconstriction induced by the excitation of vascular postsynaptic alpha 2 adrenoceptors. The inhibitory effect of calcium entry blockers is reversed by the calcium entry promoter Bay k 8644. The vasoconstriction induced by alpha 1-adrenoceptor stimulation is less generally influenced by calcium entry blockers than the alpha 2 effects. The interference with alpha 2-adrenoceptor-induced vasoconstriction may contribute to the vasodilator action of the calcium entry blockers, especially in hypertensive patients who show a hyperreactivity to pressor responses toward catecholamines.
本文综述了钙通道阻滞剂的降压作用机制。其降压/降血压作用的主要背景是毛细血管前小动脉（阻力血管）扩张，这会导致总外周阻力降低，进而使血压下降。血管舒张是由跨膜钙内流的抑制引起的，可能还与钙调蛋白的干扰有关，不过这种干扰作用可能较小。钙通道阻滞剂能显著降低血管突触后α₂肾上腺素能受体兴奋所诱导的血管收缩。钙通道促进剂Bay k 8644可逆转钙通道阻滞剂的抑制作用。与α₂效应相比，α₁肾上腺素能受体刺激所诱导的血管收缩受钙通道阻滞剂的影响通常较小。对α₂肾上腺素能受体诱导的血管收缩的干扰可能有助于钙通道阻滞剂的血管舒张作用，尤其是在对儿茶酚胺升压反应表现出高反应性的高血压患者中。
