Published online before print May 7, 2007, doi: 10.1161/HYPERTENSIONAHA.106.086587
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(Hypertension. 2007;50:33.)
© 2007 American Heart Association, Inc.
Editorial Commentaries |
Angiotensin Receptors and Aging
From the Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia School of Medicine, Charlottesville.
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. |
The major biological actions of the renin–angiotensin system are mediated by angiotensin (Ang) II, which binds with equal affinity to Ang type 1 (AT1) and type 2 (AT2) receptors. The majority of Ang II actions, however, are mediated by the AT1 receptor, including vasoconstriction, cellular proliferation, tissue growth, direct renal tubular sodium reabsorption, sympathetic nervous stimulation, and aldosterone secretion, which, in aggregate, lead to a rise in blood pressure.1 Because the AT1 receptor is expressed ubiquitously in relatively high levels at renal and cardiovascular sites, an increase in blood pressure represents the net response to increased circulating Ang II.
By contrast, AT2 receptors carry a relatively low level of tissue expression in the adult compared with that of AT1 receptors.1 AT2 receptors are expressed in large quantities in fetal tissues, but their expression decreases in the neonatal period and reaches a comparatively low level in the adult animal. However, the capacity for AT2 receptor re-expression is retained in the adult, because upregulation is a common response to circumstances of cardiovascular tissue damage, such as myocardial infarction, heart failure, and hypertension.
Activation of AT2 receptors by the binding of Ang II stimulates a hormonal cascade consisting of bradykinin (BK), NO, and cGMP, leading to vasodilation that is counterregulatory to the vasoconstriction induced by Ang II via AT1 receptors.2 AT2 receptor–induced vasodilation has been unequivocally demonstrated in both resistance and capacitance vessels.3,4 In capacitance vessels, Ang II binding to the AT2 receptor activates the BK B2 receptor, stimulating the phosphorylation
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