Gouw M A, Wilffert B, van Zwieten P A
Division of Pharmacotherapy/Pharmacology, Academic Medical Centre, University of Amsterdam, The Netherlands.
Pharmacology. 1989;38(5):289-97. doi: 10.1159/000138549.
We investigated the inhibitory effect of the calcium entry blockers (CEBs) nifedipine, diltiazem, flunarizine and gallopamil on K+-and serotonin (5-HT)-induced contractions of the rat jugular vein and aorta in vitro. In both tissues all four CEBs inhibited K+-induced contractions concentration-dependently in a similar manner in the same concentration range. Only a smaller contraction due to hyperosmolarity of the medium as the result of addition of 100 mmol/l KCl persisted. 5-HT-induced contractions were antagonized more strongly by nifedipine than by diltiazem and flunarizine, suggesting different sites of action. Moreover, the arterial preparation proved to be more sensitive to CEB pretreatment than the jugular vein preparation. Gallopamil influenced 5-HT-induced contractions also by an antiserotonergic effect.
我们研究了钙通道阻滞剂（CEBs）硝苯地平、地尔硫䓬、氟桂利嗪和加洛帕米对体外培养的大鼠颈静脉和主动脉中钾离子（K⁺）及5-羟色胺（5-HT）诱导收缩的抑制作用。在这两种组织中，所有四种CEBs在相同浓度范围内，以相似的方式浓度依赖性地抑制K⁺诱导的收缩。仅因添加100 mmol/l KCl导致的介质高渗引起的较小收缩持续存在。硝苯地平对5-HT诱导的收缩的拮抗作用比对地尔硫䓬和氟桂利嗪更强，提示作用位点不同。此外，动脉标本对CEB预处理的敏感性高于颈静脉标本。加洛帕米对5-HT诱导的收缩的影响也通过抗5-羟色胺能效应实现。
