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 survey

101 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)796-799
Number of pages4
JournalHypertension
Volume44
Issue number6
DOIs
StatePublished - Dec 1 2004

Fingerprint

rho-Associated Kinases
Hypertension
Myosin-Light-Chain Phosphatase
Contractile Proteins
Myosin Light Chains
Calmodulin
Vasoconstriction
Vascular Smooth Muscle
Vasodilation
Angiotensin II
Adrenergic Receptors
Endothelial Cells
Phosphorylation

Keywords

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

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Hypertension and RhoA/Rho-kinase signaling in the vasculature : Highlights from the recent literature. / Lee, Dexter L.; Webb, R Clinton; Jin, Liming.

In: Hypertension, Vol. 44, No. 6, 01.12.2004, p. 796-799.

Research output: Contribution to journalShort survey

@article{77638b50d7b74ace90c76346309a52f1,
title = "Hypertension and RhoA/Rho-kinase signaling in the vasculature: Highlights from the recent literature",
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.",
keywords = "Muscle, smooth, Nitric oxide, Signal transduction, Vasculature, Vasoconstriction",
author = "Lee, {Dexter L.} and Webb, {R Clinton} and Liming Jin",
year = "2004",
month = "12",
day = "1",
doi = "10.1161/01.HYP.0000148303.98066.ab",
language = "English (US)",
volume = "44",
pages = "796--799",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Hypertension and RhoA/Rho-kinase signaling in the vasculature

T2 - Highlights from the recent literature

AU - Lee, Dexter L.

AU - Webb, R Clinton

AU - Jin, Liming

PY - 2004/12/1

Y1 - 2004/12/1

N2 - 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.

AB - 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.

KW - Muscle, smooth

KW - Nitric oxide

KW - Signal transduction

KW - Vasculature

KW - Vasoconstriction

UR - http://www.scopus.com/inward/record.url?scp=9644280885&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=9644280885&partnerID=8YFLogxK

U2 - 10.1161/01.HYP.0000148303.98066.ab

DO - 10.1161/01.HYP.0000148303.98066.ab

M3 - Short survey

VL - 44

SP - 796

EP - 799

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 6

ER -