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Am J Physiol Heart Circ Physiol 274: H868-H873, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 3, H868-H873, March 1998

Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors

Masayoshi Hamawaki1, Thomas M. Coffman3, Andrew Lashus1, Masaaki Koide1, Michael R. Zile1,2, Michael I. Oliverio3, Gilberto Defreyte1, George Cooper IV1,2, and Blase A. Carabello1,2

1 Cardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston 29425; 2 Ralph H. Johnson Department of Veterans Affairs, Charleston, South Carolina 29403; and 3 Nephrology Section, Durham Medical Center, Durham, North Carolina 27705

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-angiotensin system was not an obligate factor in cardiac hypertrophy. We examined the left ventricular hypertrophic response to a pressure overload in mice devoid of the AT1A receptor, the putative major effector of the growth response of the renin-angiotensin system. Aortic banding produced similar transband gradients in wild-type and AT1A 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 hypertrophy is not affected by the absence of the AT1A receptor and its signaling pathway and that this component of the renin-angiotensin system is not necessary in cardiac hypertrophy.

renin-angiotensin system; aortic stenosis; gene expression; ventricular function


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