Arterial response to shear stress critically depends on endothelial TRPV4 expression.

ABSTRACT:

Background

In blood vessels, the endothelium is a crucial signal transduction interface in control of vascular tone and blood pressure to ensure energy and oxygen supply according to the organs' needs. In response to vasoactive factors and to shear stress elicited by blood flow, the endothelium secretes vasodilating or vasocontracting autacoids, which adjust the contractile state of the smooth muscle. In endothelial sensing of shear stress, the osmo- and mechanosensitive Ca(2+)-permeable TRPV4 channel has been proposed to be candidate mechanosensor. Using TRPV4(-/-) mice, we now investigated whether the absence of endothelial TRPV4 alters shear-stress-induced arterial vasodilation.

Methodology/principal findings

In TRPV4(-/-) mice, loss of the TRPV4 protein was confirmed by

SUBMITTER: Hartmannsgruber V 

PROVIDER: S-EPMC1959246 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature