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.
Duke Scholars
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Related Subject Headings
- Renin
- Receptors, Angiotensin
- Receptor, Angiotensin, Type 1
- Mice, Knockout
- Mice
- Heterozygote
- Cardiovascular System & Hematology
- Cardiomegaly
- Body Weight
- Blood Pressure
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Renin
- Receptors, Angiotensin
- Receptor, Angiotensin, Type 1
- Mice, Knockout
- Mice
- Heterozygote
- Cardiovascular System & Hematology
- Cardiomegaly
- Body Weight
- Blood Pressure