Levy J V
Res Commun Chem Pathol Pharmacol. 1975 Jul;11(3):387-404.
The vulnerability of aortic strips from 50-52 week old Spontaneously Hypertensive Rats (SHR) and normotensive Wistar-Kyoto (WKY) controls to the inhibitory or relaxing effects of the calcium antagonists verapamil and diazoxide was studied. Verapamil produced concentration-dependent inhibition (antagonism) of KCl, PGE2, and methoxamine-induced contraction of aortic strips from SHR and WKY. KCl and PGE2-induced contraction of SHR tissue were less readily antagonized by verapamil compared to WKY preparations. The reverse was seen with methoxamine-induced contraction. The slope of the verapamil inhibition curve of KCl-induced contraction was significantly steeper for aortic strips form WKY. Verapamil and diazoxide also produced concentration-dependent relaxation of KCl-induced contraction of aortic strips, no significant differences being noted in SHR and WKY responses. Results are compatible with the hypothesis that arterial smooth muscle from SHR is characterized by a more tightly bound pool or source of activator Ca++ which is released by certain agonists. Failure to observe a significant difference in verapamil or diazoxide induced relaxation of KCl contracted tissues from SHR or WKY suggests that in the tonic phase of KCl contraction, transmembrane fluxes of Ca++ in SHR and WKY are equally vulnerable to the Ca++ channel inhibitory effect of the antagonists.
研究了50 - 52周龄自发性高血压大鼠（SHR）和正常血压的Wistar - Kyoto（WKY）对照大鼠的主动脉条对钙拮抗剂维拉帕米和二氮嗪的抑制或舒张作用的敏感性。维拉帕米对SHR和WKY的主动脉条由氯化钾、前列腺素E2和甲氧明诱导的收缩产生浓度依赖性抑制（拮抗作用）。与WKY制剂相比，维拉帕米对SHR组织中由氯化钾和前列腺素E2诱导的收缩的拮抗作用较弱。甲氧明诱导的收缩情况则相反。WKY主动脉条由氯化钾诱导收缩的维拉帕米抑制曲线斜率明显更陡。维拉帕米和二氮嗪也使氯化钾诱导的主动脉条收缩产生浓度依赖性舒张，SHR和WKY的反应未观察到显著差异。结果与以下假设相符：SHR的动脉平滑肌的特征是存在一个结合更紧密的激活剂Ca++池或来源，其由某些激动剂释放。未观察到维拉帕米或二氮嗪对SHR或WKY的氯化钾收缩组织诱导的舒张有显著差异，这表明在氯化钾收缩的强直期，SHR和WKY中Ca++的跨膜通量对拮抗剂的Ca++通道抑制作用同样敏感。
