RhoA/rho-kinase, vascular changes, and hypertension

Kanchan Chitaley, David S. Weber, R. Clinton Webb

Research output: Contribution to journalArticle

65 Scopus citations

Abstract

Hypertension, the result of a sustained increase in vascular peripheral resistance, is partly due to vascular remodeling and increased vasoconstrictor sensitivity. Stimulation of heterotrimeric G-protein-coupled receptors by various contractile agonists activates intracellular signaling molecules to result in an increase in cytosolic Ca++ and the subsequent phosphorylation of myosin light chain by Ca++/calmodulin-dependent myosin light chain kinase. Additionally, a portion of a-adrenergic, serotonergic, and endothelin-1-induced contraction is partially mediated by the calcium-independent activation of the small G-protein RhoA and of a downstream target, Rho-kinase. Isolated arteries from hypertensive animals have been shown to have an increased contractile sensitivity to various agonists and to exhibit evidence of remodeling. Recent data suggest that some of these vascular changes may be mediated by increased activity of RhoA/Rho-kinase, potentially introducing a novel therapeutic approach for the treatment of hypertension.

Original languageEnglish (US)
Pages (from-to)139-144
Number of pages6
JournalCurrent Hypertension Reports
Volume3
Issue number2
DOIs
Publication statusPublished - Jan 1 2001

    Fingerprint

ASJC Scopus subject areas

  • Internal Medicine

Cite this