ROLE OF NO IN VASCULAR SMOOTH-MUSCLE AND CARDIAC-MUSCLE FUNCTION

被引:95
作者
SCHULZ, R
TRIGGLE, CR
机构
[1] UNIV ALBERTA,FAC MED,DEPT PHARMACOL,EDMONTON T6G 2S2,AB,CANADA
[2] UNIV CALGARY,FAC MED,ALBERT HEART & STROKE CHAIR CARDIOVASC RES,DEPT PHARMACOL & THERAPEUT,CALGARY T2N 4N1,AB,CANADA
[3] UNIV CALGARY,FAC MED,SMOOTH MUSCLE GRP,CALGARY T2N 4N1,AB,CANADA
[4] UNIV CALGARY,FAC MED,CIBA GEIGY CANADA,CALGARY T2N 4N1,AB,CANADA
关键词
D O I
10.1016/0165-6147(94)90321-2
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
NO is a key transducer of a vasodilator message from the endothelium to vascular smooth muscle. Recently, its actions as a negative inotrope in cardiac muscle have been discovered. In the vasculature, it is synthesized under physiological conditions following activation of a low-output, Ca2+-dependent NO synthase (NOS) in endothelial cells. Immune activation triggers the expression of a high-output, Ca2+-independent NOS in the vasculature and myocardium, causing the overproduction of N0 and significant cardiovascular dysfunction. In this article, Richard Schulz and Chris Triggle briefly review recent findings concerning the role of NO, and other endothelium-derived factors, in vascular smooth muscle function and consider the consequences of its production in the heart.
引用
收藏
页码:255 / 259
页数:5
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