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 Ca<sup>2+</sup>/calmodulin-dependent isoform, can be activated by shear stress and isometric contraction in the absence of a maintained increase in [Ca<sup>2+</sup>]<sub>i</sub> 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 Ca<sup>2+</sup>-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.
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Dates
Type | When |
---|---|
Created | 22 years, 4 months ago (April 15, 2003, 5:24 a.m.) |
Deposited | 4 months, 1 week ago (April 23, 2025, 11:49 p.m.) |
Indexed | 3 months, 1 week ago (May 23, 2025, 7:26 p.m.) |
Issued | 27 years, 7 months ago (Jan. 1, 1998) |
Published | 27 years, 7 months ago (Jan. 1, 1998) |
Published Online | 27 years, 4 months ago (April 16, 1998) |
Published Print | 27 years, 7 months ago (Jan. 1, 1998) |
@article{Busse_1998, title={Pulsatile Stretch and Shear Stress: Physical Stimuli Determining the Production of Endothelium-Derived Relaxing Factors}, volume={35}, ISSN={1423-0135}, url={http://dx.doi.org/10.1159/000025568}, DOI={10.1159/000025568}, number={2}, journal={Journal of Vascular Research}, publisher={S. Karger AG}, author={Busse, Rudi and Fleming, Ingrid}, year={1998}, pages={73–84} }