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

Publication ,  Journal Article
Hamawaki, M; Coffman, TM; Lashus, A; Koide, M; Zile, MR; Oliverio, MI; DeFreyte, G; Cooper, G; Carabello, BA
Published in: Am J Physiol
March 1998

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

Published In

Am J Physiol

DOI

ISSN

0002-9513

Publication Date

March 1998

Volume

274

Issue

3

Start / End Page

H868 / H873

Location

United States

Related Subject Headings

  • Renin
  • Receptors, Angiotensin
  • Receptor, Angiotensin, Type 1
  • Mice, Knockout
  • Mice
  • Heterozygote
  • Cardiovascular System & Hematology
  • Cardiomegaly
  • Body Weight
  • Blood Pressure
 

Citation

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Hamawaki, M., Coffman, T. M., Lashus, A., Koide, M., Zile, M. R., Oliverio, M. I., … Carabello, B. A. (1998). Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors. Am J Physiol, 274(3), H868–H873. https://doi.org/10.1152/ajpheart.1998.274.3.H868
Hamawaki, M., T. M. Coffman, A. Lashus, M. Koide, M. R. Zile, M. I. Oliverio, G. DeFreyte, G. Cooper, and B. A. Carabello. “Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors.Am J Physiol 274, no. 3 (March 1998): H868–73. https://doi.org/10.1152/ajpheart.1998.274.3.H868.
Hamawaki M, Coffman TM, Lashus A, Koide M, Zile MR, Oliverio MI, et al. Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors. Am J Physiol. 1998 Mar;274(3):H868–73.
Hamawaki, M., et al. “Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors.Am J Physiol, vol. 274, no. 3, Mar. 1998, pp. H868–73. Pubmed, doi:10.1152/ajpheart.1998.274.3.H868.
Hamawaki M, Coffman TM, Lashus A, Koide M, Zile MR, Oliverio MI, DeFreyte G, Cooper G, Carabello BA. Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors. Am J Physiol. 1998 Mar;274(3):H868–H873.

Published In

Am J Physiol

DOI

ISSN

0002-9513

Publication Date

March 1998

Volume

274

Issue

3

Start / End Page

H868 / H873

Location

United States

Related Subject Headings

  • Renin
  • Receptors, Angiotensin
  • Receptor, Angiotensin, Type 1
  • Mice, Knockout
  • Mice
  • Heterozygote
  • Cardiovascular System & Hematology
  • Cardiomegaly
  • Body Weight
  • Blood Pressure