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Hypertension. 2006;48:824-825
Published online before print October 2, 2006, doi: 10.1161/01.HYP.0000244109.55948.bc
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(Hypertension. 2006;48:824.)
© 2006 American Heart Association, Inc.


Editorial Commentaries

Role of Angiotensin Type 2 Receptors in Vasodilation of Resistance and Capacitance Vessels

Robert M. Carey; Jennifer Park

From the Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, Charlottesville, Va.

Correspondence to Robert M. Carey, PO Box 801414, University of Virginia Health System, Charlottesville, VA 22908-1414. E-mail rmc4c@virginia.edu


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

Angiotensin II (Ang II), the major effector component of the renin-angiotensin system, has an important regulatory role in cardiovascular and renal function. Ang II exerts its actions by binding with equal affinity to angiotensin type 1 (AT1) and type 2 (AT2) receptors.1 The predominant receptor subtype found in the vasculature of adults is the AT1 receptor. Ang II activation of AT1 receptors induces vasoconstriction, cellular proliferation, tissue growth, renal sodium retention, sympathetic nervous system stimulation, and aldosterone secretion, the integrated response of which leads to increased blood pressure.1 The AT2 receptor is expressed in large quantities in the fetus and decreases markedly after birth but is still present in low amounts in adult tissues.1,2 AT2 receptors are upregulated under conditions associated with cardiovascular tissue damage, such as myocardial infarction, heart failure, and hypertension.3 The relatively low expression level of AT2 receptors compared with that of AT1 receptors is a major reason why the actions and cell signaling mechanisms of AT1 receptors are well characterized compared with those of AT2 receptors.

Ang II binding to AT2 receptors activates a counterregulatory pathway whereby vasoconstriction mediated by AT1 receptors is opposed by AT2 receptor–induced vasodilation.4,5 AT2 receptor–mediated vasodilation has now been demonstrated in a large variety of resistance vessels including the mesenteric, uterine, renal, coronary, and cerebral vascular beds.6–10 The integrated counterregulatory response to AT2 receptor activation can be unmasked in normal and hypertensive animals in which, when AT1 receptors are blocked, exogenous Ang II induces hypotension that is abolished by . . . [Full Text of this Article]


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