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
收藏
页码：355 / 358
页数：4
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