TY - JOUR
T1 - RhoA/rho-kinase, vascular changes, and hypertension
AU - Chitaley, Kanchan
AU - Weber, David S.
AU - Webb, R. Clinton
N1 - Funding Information:
This work was supported by NIH grant HL18575. Kanchan Chitaley is the recipient of support from a NIH training grant for Systems and Integrative Physiology (2-T-32-GM083221). Dr. David Weber is a postdoctoral fellow of the American Heart Association.
PY - 2001
Y1 - 2001
N2 - 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.
AB - 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.
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U2 - 10.1007/s11906-001-0028-4
DO - 10.1007/s11906-001-0028-4
M3 - Article
C2 - 11276396
AN - SCOPUS:0035315803
SN - 1522-6417
VL - 3
SP - 139
EP - 144
JO - Current Hypertension Reports
JF - Current Hypertension Reports
IS - 2
ER -