Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors.

Abstract:

:Mechanical forces generated at the endothelium by fluid shear stress and pulsatile stretch are important in ensuring the continuous release of vasoactive endothelial autacoids. Although the mechanism by which endothelial cells are able to detect and convert these physical stimuli into chemical signals is unclear, this process involves the activation of integrins, G proteins and cascades of protein kinases. The constitutive endothelial nitric oxide synthase (NOS III), classified as a Ca2+/calmodulin-dependent isoform, can be activated by shear stress and isometric contraction in the absence of a maintained increase in [Ca2+]i via a mechanism involving its redistribution within the cytoskeleton/caveolae and the activation of one or more regulatory NOS-associated proteins. Thus it would appear that the intracellular cascades activated by Ca2+-elevating receptor-dependent agonists, such as bradykinin, and hemodynamic stimuli are distinct. Rhythmic vessel distension is also able to elicit the synthesis of superoxide anions and the endothelium-derived hyperpolarizing factor which play a role in modulating arterial compliance in certain vascular beds.

journal_name

J Vasc Res

authors

Busse R,Fleming I

doi

10.1159/000025568

subject

Has Abstract

pub_date

1998-03-01 00:00:00

pages

73-84

issue

2

eissn

1018-1172

issn

1423-0135

pii

jvr35073

journal_volume

35

pub_type

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