FIGURE 4.1. Under control conditions, ECs respond to receptor-dependent dilators and shear stress by producing NO via calcium-calmodulin-dependent activation of nitric oxide synthase.

FIGURE 4.1

Under control conditions, ECs respond to receptor-dependent dilators and shear stress by producing NO via calcium-calmodulin-dependent activation of nitric oxide synthase. The NO diffuses into the underlying smooth muscle cell to activate guanylate cyclase, which generates cGMP to reduce intracellular calcium. The net result is smooth muscle relaxation and vessel dilation. During inflammation, cytokines and other mediators activate endothelial NADPH oxidase (and other oxidases) to produce superoxide (O2), which inactivates NO and diminishes the capacity of receptor-dependent agonists and shear stress to elicit dilation in arterioles.

From: Chapter 4, Impaired Vasomotor Responses

Cover of Inflammation and the Microcirculation
Inflammation and the Microcirculation.
Granger DN, Senchenkova E.
San Rafael (CA): Morgan & Claypool Life Sciences; 2010.
Copyright © 2010 by Morgan & Claypool Life Sciences.

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