van Zwieten P A, Timmermans P B
Division of Pharmacotherapy, Amsterdam, The Netherlands.
Ann N Y Acad Sci. 1988;522:351-60. doi: 10.1111/j.1749-6632.1988.tb33376.x.
A survey is given of the interaction between alpha-adrenoceptor-triggered vasoconstriction and the influx of extracellular calcium ions. This problem was investigated by studying the influence of calcium entry blockers (CEB) on the vasoconstriction induced by several types of alpha 2- and alpha 1-adrenoceptor agonists both in vivo and in vitro. In addition, experiments were performed with the calcium entry promoter Bay K 8644. alpha 2-Adrenoceptor-triggered vasoconstriction is invariably accompanied by an influx of extracellular calcium ions which substantially contributes to the initiation of vascular smooth muscle contraction. This concept is a very general phenomenon, which holds for a variety of alpha 2-adrenoceptor agonists and CEB, in vivo and in vitro, and in different animal species. The alpha 1-adrenoceptor-induced vasoconstriction appears to be caused both by the release of intracellular calcium and by the transmembranous influx of intracellular calcium. The ratio between both processes is very different, depending upon the type of alpha 1-adrenoceptor agonist and on the experimental preparation used. It has been speculated that this ratio can be influenced by phenoxybenzamine.
本文综述了α-肾上腺素能受体触发的血管收缩与细胞外钙离子内流之间的相互作用。通过研究钙通道阻滞剂（CEB）对多种α2-和α1-肾上腺素能受体激动剂在体内和体外诱导的血管收缩的影响，对该问题进行了研究。此外，还使用钙通道促进剂Bay K 8644进行了实验。α2-肾上腺素能受体触发的血管收缩总是伴随着细胞外钙离子的内流，这在很大程度上促进了血管平滑肌收缩的起始。这一概念是一种非常普遍的现象，适用于多种α2-肾上腺素能受体激动剂和CEB，在体内和体外以及不同动物物种中均如此。α1-肾上腺素能受体诱导的血管收缩似乎是由细胞内钙的释放和细胞内钙的跨膜内流共同引起的。这两个过程之间的比例差异很大，这取决于α1-肾上腺素能受体激动剂的类型和所使用的实验制剂。据推测，这种比例可能会受到酚苄明的影响。
