PRESSURE-OVERLOAD HYPERTROPHY IS UNABATED IN MICE DEVOID OF AT(1A) RECEPTORS

Mechanisms controlling cardiac growth are under intense investigation. Among these, the renin-angiotensin system has received great interest . In the current study, we tested the hypothesis that the renin-angiot ensin system was not an obligate factor in cardiac hypertrophy. We exa mined the left, ventricular hypertrophic response to a pressure overlo ad in mice devoid of the AT(1A) receptor the putative major effector o f the growth response of the renin-angiotensin system. Aortic banding produced similar transband gradients in wild-type and AT(1A) knockout mice. The left ventricular mass-to-body weight ratio increased from 3. 44 +/- 0.08 to 5.62 +/- 0.25 in wild-type ascending aortic-banded mice . The response in the knockout mice was not different (from 2.97 +/- 0 .13 to 5.24 +/- 0.37). We conclude that the magnitude of cardiac hyper trophy is not affected by the absence of the AT(1A) receptor and its s ignaling pathway and that this component of the renin-angiotensin syst em is not necessary in cardiac hypertrophy.