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Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system.

Authors :
Mehta, Puja K.
Griendling, Kathy K.
Source :
American Journal of Physiology: Cell Physiology. Jan2007, Vol. 292 Issue 1, pC82-C97. 16p. 4 Diagrams, 1 Chart.
Publication Year :
2007

Abstract

The renin-angiotensin system is a central component of the physiological and pathological responses of cardiovascular system. Its primary effector hormone, angiotensin II (ANG II), not only mediates immediate physiological effects of vasoconstriction and blood pressure regulation, but is also implicated in inflammation, endothelial dysfunction, atherosclerosis, hypertension, and congestive heart failure. The myriad effects of ANG II depend on time (acute vs. chronic) and on the cells/tissues upon which it acts. In addition to inducing G protein- and non-G protein-related signaling pathways, ANG II, via AT1 receptors, carries out its functions via MAP kinases (ERK 1/2, JNK, p38MAPK), receptor tyrosine kinases [PDGF, EGFR, insulin receptor], and nonreceptor tyrosine kinases [Src, JAK/STAT, focal adhesion kinase (FAK)]. AT1R-mediated NAD(P)H oxidase activation leads to generation of reactive oxygen species, widely implicated in vascular inflammation and fibrosis. ANG II also promotes the association of scaffolding proteins, such as paxillin, talin, and p130Cas, leading to focal adhesion and extracellular matrix formation. These signaling cascades lead to contraction, smooth muscle cell growth, hypertrophy, and cell migration, events that contribute to normal vascular function, and to disease progression. This review focuses on the structure and function of AT1 receptors and the major signaling mechanisms by which angiotensin influences cardiovascular physiology and pathology. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03636143
Volume :
292
Issue :
1
Database :
Academic Search Index
Journal :
American Journal of Physiology: Cell Physiology
Publication Type :
Academic Journal
Accession number :
23802065
Full Text :
https://doi.org/10.1152/ajpcell.00287.2006