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Cardiovascular Research 2004 62(3):460-467; doi:10.1016/j.cardiores.2004.01.011
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Cardiovascular and renal function of angiotensin II type-2 receptors

Olaf Jöhren*, Andreas Dendorfer and Peter Dominiak

Institute of Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany

* Corresponding author. Tel.: +49-451-500-4357; fax: +49-451-500-3327. Email address: joehren{at}uni-luebeck.de

While all of the well-known cardiovascular and renal effects of angiotensin II (ANG) are attributed to the ANG type-1 (AT1) receptor, much less is known about the function of ANG type-2 (AT2) receptors. This review focuses on progress made in AT2 receptor research over the past 10 years mainly enabled by the availability of AT2 receptor-deficient mice. Two general mechanisms regarding AT2 receptor-mediated actions emerge from recent experiments. Firstly, AT2 receptor stimulation inhibits growth and promotes apoptosis, an important mechanism during development and tissue remodeling. Secondly, ANG stimulates the release of nitric oxide (NO)/cGMP via AT2 receptor activation, as described in the aorta, heart, and kidney. This effect appears to be indirectly mediated by the modulation of bradykinin release. Thus, activation of AT2 receptors may be potentially protective and appears to oppose the effects mediated by AT1 receptors. The question whether AT2 receptors are activated in patients with elevated ANG levels when treated with AT1 receptor antagonists and whether these effects are relevant awaits further clarification.

KEYWORDS Angiotensin; AT2 receptor; Gene deficiency; Apoptosis; Renal function

Time for primary review 29 days


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