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(Hypertension. 2004;44:796.)
© 2004 American Heart Association, Inc.

Hypertension Highlights

Hypertension and RhoA/Rho-Kinase Signaling in the Vasculature

Highlights From the Recent Literature

From the Department of Physiology, Medical College of Georgia, Augusta.

Correspondence to Liming Jin, Department of Physiology, Medical College of Georgia, 1120 15th St, Augusta, GA 30912-3000. E-mail ljin{at}mcg.edu

Abstract

Under normal conditions, contractile activity in vascular smooth muscle is initiated by either receptor activation (norepinephrine, angiotensin II, etc.) or by a stretch-activated mechanism. After this activation, several signaling pathways can initiate a Ca²⁺-calmodulin interaction to stimulate phosphorylation of the light chain of myosin. Ca²⁺ sensitization of the contractile proteins is signaled by the RhoA/Rho-kinase pathway to inhibit the dephosphorylation of the light chain by myosin phosphatase thereby maintaining force generation. In opposition to force generation, NO is released from endothelial cells and causes vasodilation through inhibition of the RhoA/Rho-kinase signaling pathway. This brief review will highlight recent studies demonstrating a role for the RhoA/Rho-kinase signaling pathway in the increased vasoconstriction characteristic of hypertension.

Key Words: vasculature • signal transduction • muscle, smooth • nitric oxide • vasoconstriction

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