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(Hypertension. 2007;49:953.)
© 2007 American Heart Association, Inc.

Brief Reviews

Angiotensin II Type 1 Receptor Gene Regulation

Transcriptional and Posttranscriptional Mechanisms

From the Davis Heart and Lung Research Institute, Ohio State University, Columbus.

Correspondence to Terry S. Elton, Davis Heart and Lung Research Institute, Ohio State University, DHLRI 515, 473 West 12th Ave, Columbus, OH 43210. E-mail terry.elton@osumc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Angiotensin II (Ang II), the major bioactive peptide of the renin–angiotensin system, was originally described as a potent vasoconstrictor. It is now recognized as a multifunctional hormone influencing many cellular processes, including cell growth, apoptosis, migration, inflammation, and fibrosis.^1,2 Under pathological conditions, the vasoconstrictor, mitogenic, proinflammatory, and profibrotic actions of Ang II contribute to altered vascular tone, structural remodeling, and endothelial dysfunction.^3–6 Thus, Ang II plays a key role in the pathogenesis of cardiovascular diseases.

The biological responses of Ang II are mediated by its interaction with 2 distinct high-affinity G protein–coupled receptors now designated Ang II type 1 receptor (AT₁R) and Ang II type 2 receptor.⁷ Most of the known physiological and pathophysiological effects of Ang II are mediated via the AT₁R.^1–7 This receptor subtype is expressed in cardiovascular-relevant cell types including vascular smooth muscle cells (VSMCs), endothelial cells, cardiac myocytes, cardiac fibroblasts, and renal mesangial cells.⁷ The multiple actions of Ang II, mediated through the AT₁R, are a result of complex intracellular signaling pathways including stimulation of the phospholipase C/inositol 1,4,5-trisphosphate/diacylglycerol cascade, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinases, tyrosine kinases, and RhoA/Rho kinase.^1,2,4,6,7 In addition, AT₁Rs mediate many of their pathophysiological effects by stimulating reactive oxygen species generation via an reduced nicotinamide-adenine dinucleotide/reduced nicotinamide-adenine dinucleotide phosphate oxidase-dependent mechanism.^2,8 Reactive oxygen species, in turn, influences downstream signaling molecules, including transcription factors, tyrosine kinases/phosphatases, Ca²⁺ channels, and MAPKs.^2,8

The expression level of the AT₁R defines the biological efficacy of Ang II; hence, overexpression of the . . . [Full Text of this Article]

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