Hypertension and RhoA/Rho-kinase signaling in the vasculature: Highlights from the recent literature

Dexter L. Lee, R. Clinton Webb, Liming Jin

Research output: Contribution to journalShort surveypeer-review

113 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)796-799
Number of pages4
Issue number6
StatePublished - Dec 2004
Externally publishedYes


  • Muscle, smooth
  • Nitric oxide
  • Signal transduction
  • Vasculature
  • Vasoconstriction

ASJC Scopus subject areas

  • Internal Medicine


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