EFFECTS OF VASOPRESSIN ON PHOSPHOINOSITIDE HYDROLYSIS AND MYOCARDIAL-CONTRACTILITY

被引：16

作者：

ENDOH, M

TAKANASHI, M

NOROTA, I

机构：

[1] Department of Pharmacology, Yamagata University School of Medicine, Yamagata

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 1992年 / 218卷 / 2-3期

关键词：

VASOPRESSIN; PHOSPHOINOSITIDE (PI) HYDROLYSIS; ALPHA-1-ADRENOCEPTORS; ENDOTHELIN; NONPEPTIDE V1-RECEPTOR ANTAGONISTS; VENTRICULAR MYOCARDIUM (RABBIT);

D O I：

10.1016/0014-2999(92)90192-7

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The effects of vasopressin on phosphoinositide hydrolysis, ventricular contractility and adrenoceptor-mediated inotropy were studied in the rabbit. Vasopressin caused an accumulation of [H-3]inositol monophosphate in ventricular slices prelabelled with myo-[H-3]inositol, whereas it elicited a small but definite negative inotropic effect. In addition, vasopressin attenuated the positive inotropic effect elicited via alpha-1- and endothelin receptors without affecting the beta-adrenoceptor-mediated effect. The nonpeptide-selective V1 receptor antagonist OPC 21268 (a quinolinone derivative) inhibited the vasopressin-induced accumulation of [H-3]inositol monophosphate. The present results indicate that vasopressin stimulates phosphoinositide hydrolysis via V1 receptors, but inhibits force and the alpha-1-mediated positive inotropic effect in the rabbit ventricular myocardium.

引用

页码：355 / 358

页数：4

共 8 条

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