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Vasopressor peptides and depolarization stimulated Ca2+-entry into cultured vascular smooth muscle.

作者信息

Zschauer A, Scott-Burden T, Bühler F R, van Breemen C

机构信息

Department of Research, University Hospital, Basel, Switzerland.

出版信息

Biochem Biophys Res Commun. 1987 Oct 14;148(1):225-31. doi: 10.1016/0006-291x(87)91099-0.

Abstract

45Ca-uptake was measured in monolayers of cultured rat aortic smooth muscle cells. Sufficient extracellular 45Ca could be removed by a 90 second cold La3+ was to reveal stimulation of 45Ca-uptake by high K+-depolarization and the vasopressor peptides angiotensin II and vasopressin. The high K+-stimulated 45Ca-influx was blocked by a dihydropyridine-type Ca2+-antagonist while that stimulated by angiotensin II or vasopressin was not. The 45Ca-influx stimulated by high K+-depolarization was additive to that stimulated by angiotensin II. Vasopressin and angiotensin II stimulated 45Ca-fluxes were not additive. It is concluded that vasopressor peptides stimulate Ca2+-entry through receptor operated Ca2+-channels which are distinct from voltage gated Ca2+-channels.

摘要

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