Does targeted deletion of the angiotensin II type 2 receptor prevent left ventricular hypertrophy in response to pressure overload in mice?
Targeted deletion of the AT2 receptor in mice prevents pressure overload-induced left ventricular hypertrophy, suggesting AT2 mediates hypertrophy potentially via p70(S6k).
The pathophysiological roles of the angiotensin II type 2 receptor (AT(2)) in cardiac hypertrophy remain unclear. By the targeted deletion of mouse AT(2) we were able to prevent the left ventricular hypertrophy resulting from pressure overload, while cardiac contractile functions remained normal. This implies that AT(2) is a mediator of cardiac hypertrophy in response to increased blood pressure. The effects of AT(2) deletion were independent of activation of embryonic genes for cardiac hypertrophy. However, p70(S6k), one of the key factors in cardiac hypertrophy, was markedly and specifically reduced in the ventricles of Agtr2(-)/Y mice. We propose that p70(S6k) plays a major role in AT(2)-mediated ventricular hypertrophy. This article may have been published online in advance of the print edition. The date of publication is available from the JCI website, http://www.jci.org.
Senbonmatsu et al. (Tue,) studied this question.
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