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

The American Journal of Physiology
M HamawakiB A Carabello

Abstract

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.

References

Jul 1, 1975·The Journal of Clinical Investigation·W GrossmanL P McLaurin
Sep 1, 1990·Journal of Cardiovascular Pharmacology·W ZierhutA M Gerdes
Nov 1, 1981·Circulation Research·K H MuntzJ H Mitchell
Aug 1, 1995·Circulation Research·T YamazakiK Tobe
Apr 11, 1995·Proceedings of the National Academy of Sciences of the United States of America·M ItoT M Coffman

❮ Previous
Next ❯

Citations

Nov 22, 2000·American Journal of Physiology. Heart and Circulatory Physiology·W S AkersL A Cassis
Aug 22, 2001·American Journal of Physiology. Heart and Circulatory Physiology·A NakamuraE Foster
Mar 15, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Paul BridgmanRichard D Patten
Aug 12, 2014·American Journal of Physiology. Heart and Circulatory Physiology·Jiaming LiuY James Kang
Jun 9, 2000·Annual Review of Physiology·W R MacLellan, M D Schneider
Dec 23, 2003·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Tomoko SaitoAkiyoshi Fukamizu
Mar 11, 2000·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·S A KatzL J Heller
Oct 23, 2004·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Zhongjie SunJ Robert Cade
Jan 9, 2010·Annual Review of Pharmacology and Toxicology·Michael Bader
May 17, 2003·American Journal of Physiology. Heart and Circulatory Physiology·Yuji IshibashiGeorge Cooper
Mar 22, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Jeetendra B PatelMargaret M Redfield

❮ Previous
Next ❯

Related Concepts

Related Feeds

Cardiomyopathy

Cardiomyopathy is a disease of the heart muscle, that can lead to muscular or electrical dysfunction of the heart. It is often an irreversible disease that is associated with a poor prognosis. There are different causes and classifications of cardiomyopathies. Here are the latest discoveries pertaining to this disease.

Cardiomegaly

Cardiomegaly, known as an enlarged heart, is a multifactorial disease with different pathophysiological mechanisms. Hypertension, pregnancy, exercise-induced and idiopathic causes are some mechanisms of cardiomegaly. Discover the latest research of cardiomegaly here.