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Submitted on December 27, 2004
Accepted on August 24, 2005
Department of Physiology, Faculty of Medicine, Semmelweis University, H-1444, Budapest, Hungary; Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892-4510
* To whom correspondence should be addressed. E-mail: cattk{at}mail.nih.gov.
Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst and sodium balance, and its diverse pathological actions in cardiovascular, renal, and other cell types. Ang II-induced AT1R activation via Gq/11 stimulates phospholipases A2, C, and D, and activates InsP3/Ca2+ signaling, protein kinase C isoforms, and MAP kinases, as well as several tyrosine kinases (Pyk2, Src, Tyk2, FAK), scaffold proteins (GIT1, p130Cas, paxillin, vinculin), receptor tyrosine kinases, and the NF
B pathway. The AT1R also signals via Gi/o and G11/12, and stimulates G protein-independent signaling pathways, such as 
-arrestin-mediated MAP kinase activation and the Jak/STAT pathway. Alterations in homo- or heterodimerization of the AT1R may also contribute to its pathophysiological roles. Many of the deleterious actions of AT1R activation are initiated by locally generated rather than circulating Ang II, and are concomitant with the harmful effects of aldosterone in the cardiovascular system. AT1R-mediated overproduction of reactive oxygen species (ROS) has potent growth-promoting, proinflammatory and profibrotic actions by exerting positive feedback effects that amplify its signaling in cardiovascular cells, leukocytes and monocytes. In addition to its roles in cardiovascular and renal disease, agonist-induced activation of the AT1R also participates in the development of metabolic diseases, and promotes tumor progression and metastasis through its growth-promoting and proangiogenic activities. The recognition of Ang II's pathogenic actions has led to novel clinical applications of angiotensin converting enzyme inhibitors and AT1R antagonists, in addition to their established therapeutic actions in essential hypertension.
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