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The role of arterial smooth muscle in vasorelaxation.

Abstract：

:The concept of endothelium-derived relaxing factor (EDRF) implies that nitric oxide (NO) produced by NO synthase (NOS) in the endothelium in response to vasorelaxants such as acetylcholine (ACh) acts on the underlying vascular smooth muscle cells (VSMC) inducing vascular relaxation. The EDRF concept was derived from experiments on denuded blood vessel strips and, in frames of this concept, VSMC were regarded as passive recipients of NO from endothelial cells. However, it was later found that VSMC express NOS by themselves, but the principal question remained unanswered, is the NO generation by VSMC physiologically relevant? We hypothesized that the destruction of the vascular wall anatomical integrity by rubbing off the endothelial layer might increase vascular superoxides that, in turn, reduced the NO bioactivity as a relaxing factor. To test our hypothesis, we examined ACh-induced vasorelaxation under protection against oxidative stress and found that superoxide scavengers restored vasodilatory responses to ACh in endothelium-deprived blood vessels. These findings imply that VSMC can release NO in amounts sufficient to account for the vasorelaxatory response and challenge the concept of the obligatory role of endothelial cells in the relaxation of arterial smooth muscle.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Buchwalow IB,Cacanyiova S,Neumann J,Samoilova VE,Boecker W,Kristek F

doi

10.1016/j.bbrc.2008.10.019

subject

Has Abstract

pub_date

2008-12-12 00:00:00

pages

504-507

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)01966-9

journal_volume

377

pub_type

杂志文章

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