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(Hypertension. 2005;46:1261.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

The Continuing Saga of the AT2 Receptor

A Case of the Good, the Bad, and the Innocuous

Timothy L. Reudelhuber

From the Laboratory of Molecular Biochemistry of Hypertension, Clinical Research Institute of Montreal (IRCM), Montreal, Quebec, Canada.

Correspondence to Timothy L. Reudelhuber, PhD, IRCM, 110 Pine Ave W, Montreal (QC) H2W 1R7, Canada. E-mail reudelt@ircm.qc.ca

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

Left ventricular hypertrophy (LVH) associated with hypertension puts patients at heightened risk for further cardiovascular complications. There has been lot of interest in the effects of angiotensin II on cardiac tissue because of clinical^1,2 and experimental³ evidence of LVH reversal and reduction of cardiovascular risk by inhibition of the renin-angiotensin system. Central to this question is whether angiotensin II has direct effects on the heart independent of, or in addition to, its effects on blood pressure because this might significantly modify treatment targets in certain high-risk patients. As a result, investigators in the "heart-as-a-direct-target" camp have focused a lot of energy on characterizing the cellular responses that angiotensin II triggers in the heart.

In the late 1980s, it became evident that there were 2 types of high-affinity receptors for angiotensin II that differed in pharmacological properties and tissue distribution. The angiotensin type (AT1) receptor, which mediates most of the classic cardiovascular actions of angiotensin II, was found to be a 7-transmembrane G-protein–coupled receptor. A host of signaling pathways that lead to calcium mobilization, tyrosine kinase activation, and free radical generation have been described for this receptor since its discovery. Much more controversial is the other angiotensin II type II receptor (AT2). Molecular cloning of the AT2 receptor revealed that it was only loosely related (34% identity) to the AT1 receptor. Although it is believed by many that the physiological role of the AT2 receptor is to antagonize the effects of AT1, the intracellular signaling cascade and the resulting function of . . . [Full Text of this Article]

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