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November 22, 2007AJP Heart and Circulatory Physiology

Mice expressing ACE only in the heart show that increased cardiac angiotensin II is not associated with cardiac hypertrophy

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Key result

Targeted cardiac ACE expression increasing ventricular angiotensin II twofold in mice did not produce cardiac dysfunction under basal conditions or augment cardiac hypertrophy after aortic banding.

Why the study?

Does increased local cardiac angiotensin II production promote cardiac hypertrophy or dysfunction in mice?

Population

Compound heterozygous mice with targeted ACE expression to the heart, wild-type mice, and previous ACE 8/8…

Comparison

Targeted cardiac ACE expression resulting in… vs Wild-type controls

Design

Preclinical

Follow-up

Evaluated at 6 months of age

Authors

HXHong XiaoSFSébastien FuchsEBEllen A. Bernstein

Discussion

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Overview

Moderate local Ang II elevation does not drive dysfunction or hypertrophy in mice; leaves open dose-, context-, or species-specific effects.

Structured PICO

Does increased local cardiac angiotensin II production promote cardiac hypertrophy or dysfunction in mice?

P
Population
Mice with targeted cardiac ACE expression (ACE 1/8) and wild-type controls, evaluated at 6 months of age and after aortic banding.
E
Exposure
Targeted cardiac ACE expression (ACE 1/8 model) resulting in twofold increase in ventricular angiotensin II, with or without aortic banding
C
Comparator
Wild-type controls
O
Outcome
Cardiac hypertrophy and cardiac function (assessed by echocardiography and left ventricular catheterization)surrogate

A moderate increase in local cardiac angiotensin II production does not produce cardiac dysfunction or augment pressure overload-induced cardiac hypertrophy in mice.

Cite This Study

Xiao et al. (2007) studied Cardiac hypertrophy. Targeted cardiac ACE expression (ACE 1/8 genotype) vs. Wild-type mice was evaluated on Cardiac hypertrophy and cardiac function. Targeted cardiac ACE expression increasing ventricular angiotensin II twofold in mice did not produce cardiac dysfunction under basal conditions or augment cardiac hypertrophy after aortic banding.

synapsesocial.com/papers/6a20bf956aba112f1d33798dhttps://doi.org/10.1152/ajpheart.01147.2007
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Mice Lacking Endothelial ACE2003 · 47 citations
  2. 2Over-expression of angiotensin converting enzyme-1 augments cardiac hypertrophy in transgenic rats2004 · 34 citations
  3. 3In Vivo Evidence of the Importance of Cardiac Angiotensin-Converting Enzyme in the Pathogenesis of Cardiac Hypertrophy2000 · 36 citations
  4. 4Overexpression of angiotensin AT <sub>1</sub> receptor transgene in the mouse myocardium produces a lethal phenotype associated with myocyte hyperplasia and heart block1997 · 212 citations
  5. 5Angiotensin II Induces Cardiac Phenotypic Modulation and Remodeling In Vivo in Rats1995 · 250 citations