Pressure-overload hypertrophy is unabated in mice devoid of AT1A 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-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.
Hamawaki
M
M
Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston 29425, USA.
Coffman
T M
TM
Lashus
A
A
Koide
M
M
Zile
M R
MR
Oliverio
M I
MI
DeFreyte
G
G
Cooper
G
G
Carabello
B A
BA
D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D006332:Cardiomegaly / Q000209:etiology*; D006579:Heterozygote; D051379:Mice; D018345:Mice, Knockout; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000172:deficiency*; D012083:Renin / Q000502:physiology
D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D012083:Renin