Abstract

Shear stress-induced activation of eNOS

Shear stress induced phosphorylation of eNOS

Shear stress-induced alteration in eNOS detergent solubility

Isometric contraction and eNOS activation

Summary

Discussion
Board

Mechanical forces generated at the endothelium by pulsatile blood flow are important in ensuring the continuous release of nitric oxide (NO) which modulates local vascular tone as well as cell signalling and gene expression. The constitutive endothelial NO synthase (eNOS), can be activated in response to an increase in [Ca2+]i following stimulation with receptor-dependent agonists such as acetylcholine and bradykinin. However, eNOS can also be activated by shear stress and isometric contraction in the absence of a maintained increase in [Ca2+]i via a tyrosine kinase-dependent mechanism involving its phosphorylation, redistribution within the cytoskeleton/caveolae and the activation of one or more regulatory eNOS-associated proteins.

Back to the top.
Presentation Number SAfleming0372
Keywords: nitric oxide, tyrosine kinase, shear stress, phosphorylation, calcium