Update on angiotensin AT2 receptors

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Purpose of review

This review updates major new findings and concepts introduced during the past year on the role of angiotensin II (Ang II) subtype 2 receptors (AT2Rs) in the control of blood pressure and renal function.

Recent findings

AT2R activation prevents sodium (Na+) retention and lowers blood pressure in the Ang II infusion model of experimental hypertension and prevents salt-sensitive hypertension in the obese Zucker rat model of obesity and the metabolic syndrome. Ang II metabolite, des-aspartyl1-Ang II (Ang III) is the predominant AT2R agonist in the kidney and possibly also in the vasculature; a novel synthetic Ang III peptide, β-Pro-Ang III, is vasodepressor and lowers blood pressure in conscious spontaneously hypertensive rats in the presence of low-level Ang II type 1 receptor (AT1R) blockade. Because nitric oxide is a product of AT2R activation, a potential feed-forward loop, wherein nitric oxide increases AT2R transcription, may reinforce the beneficial actions of AT2R in the long term. AT2R activation also reduces proteinuria and oxidative stress in glomerulosclerotic kidneys of high-salt obese Zucker rats.


Studies during the past year have helped to clarify the physiological and pathophysiological roles of AT2Rs and have enhanced the promise of AT2R agonists in cardiovascular and renal disease.

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