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 (AT2
Rs) in the control of blood pressure
and renal function.
R 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 AT2
R 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 (AT1
R) blockade. Because nitric oxide is a product of AT2
R activation, a potential feed-forward loop, wherein nitric oxide increases AT2
R transcription, may reinforce the beneficial actions of AT2
R in the long term. AT2
R 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 AT2
Rs and have enhanced the promise of AT2
R agonists in cardiovascular and renal disease.