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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Hamawaki, M; Coffman, TM; Lashus, A; Koide, M; Zile, MR; Oliverio, MI; DeFreyte, G; Cooper, G; Carabello, BA

Published Date

  • March 1, 1998

Published In

Volume / Issue

  • 274 / 3

Start / End Page

  • H868 - H873

PubMed ID

  • 9530198

Pubmed Central ID

  • 9530198

International Standard Serial Number (ISSN)

  • 0002-9513

Digital Object Identifier (DOI)

  • 10.1152/ajpheart.1998.274.3.H868

Language

  • eng

Conference Location

  • United States