环匹阿尼酸和雷诺丁对大鼠肠系膜动脉去极化诱导收缩的影响

Modification by cyclopiazonic acid and ryanodine of depolarization-induced constriction in rat mesenteric artery.

作者信息

Naganobu K, Takagi M, Kawasaki H, Ito K

机构信息

Department of Veterinary Pharmacology, Faculty of Agriculture, Miyazaki University, Japan.

出版信息

Eur J Pharmacol. 1994 Jan 14;251(2-3):307-10. doi: 10.1016/0014-2999(94)90415-4.

DOI:10.1016/0014-2999(94)90415-4

PMID:8149985

Abstract

Cyclopiazonic acid (53 or 159 nmol/min) or ryanodine (53 or 530 nmol/min) was applied to perfused rat mesenteric artery contracted with 40 mM K+ and 0.1 mM Ca2+. Both agents transiently elevated the perfusion pressure. The transient pressor response to caffeine observed after ryanodine was depressed more than after cyclopiazonic acid. This suggests that ryanodine increased the constriction through acceleration of Ca2+ release while cyclopiazonic acid increased it by inhibiting Ca2+ uptake into Ca2+ stores. In the continued presence of ryanodine, the next depolarization-dependent constriction was greatly depressed, suggesting that Ca(2+)-induced Ca2+ release was involved in the constriction.

摘要

向用40 mM K⁺和0.1 mM Ca²⁺收缩的灌注大鼠肠系膜动脉施加环匹阿尼酸（53或159 nmol/分钟）或ryanodine（53或530 nmol/分钟）。两种药物均使灌注压短暂升高。ryanodine处理后观察到的对咖啡因的短暂升压反应比环匹阿尼酸处理后的更受抑制。这表明ryanodine通过加速Ca²⁺释放增加收缩，而环匹阿尼酸通过抑制Ca²⁺摄取到Ca²⁺储存中来增加收缩。在持续存在ryanodine的情况下，下一次去极化依赖性收缩大大受抑制，表明Ca²⁺诱导的Ca²⁺释放参与了收缩。