What question did this study set out to answer?

To determine whether the renin-angiotensin system, specifically signaling via the AT1A receptor, is essential for pressure-overload-induced cardiac hypertrophy.

March 1, 1998AJP Heart and Circulatory Physiology

Pressure-overload hypertrophy is unabated in mice devoid of AT1Areceptors

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Why the study?

Does the absence of the AT1A receptor prevent cardiac hypertrophy in mice subjected to pressure overload?

Population

Mice devoid of the AT1A receptor (knockout) and wild-type mice

Comparison

Aortic banding in AT1A knockout mice vs Aortic banding in wild-type mice

Design

Preclinical

Authors

MHMasayoshi HamawakiNagasaki Medical Center TCThomas M. CoffmanPreventive Cardiology ALAndrew G. LashusCleveland Clinic

Discussion

Member takes

Implication

AT1A absence does not prevent pressure-overload hypertrophy in mice; leaves open non-AT1A pathways for mechanistic research.

Key Points

To determine whether the renin-angiotensin system, specifically signaling via the AT1A receptor, is essential for pressure-overload-induced cardiac hypertrophy.
Induced left ventricular pressure overload using ascending aortic banding in wild-type and AT1A receptor knockout mice.
Assessed transband pressure gradients and calculated left ventricular mass-to-body weight ratios to measure the hypertrophic response.
Aortic banding produced similar transband pressure gradients across both wild-type and AT1A knockout mice.
Left ventricular mass-to-body weight ratio increased from 3.44 ± 0.08 to 5.62 ± 0.25 in wild-type mice.
AT1A knockout mice showed an equivalent hypertrophic response, with left ventricular mass-to-body weight ratio increasing from 2.97 ± 0.13 to 5.24 ± 0.37.

Structured PICO

Does the absence of the AT1A receptor prevent cardiac hypertrophy in mice subjected to pressure overload?

Population

Mice devoid of the AT1A receptor (knockout) and wild-type mice

Intervention

Aortic banding (pressure overload) in AT1A knockout mice

Comparator

Aortic banding in wild-type mice

Outcome

Left ventricular mass-to-body weight ratiosurrogate

The AT1A receptor and its signaling pathway are not obligate factors for the development of pressure-overload cardiac hypertrophy in mice.

Cite This Study

Hamawaki et al. (1998) studied this question.

synapsesocial.com/papers/6a714bc575498292b70ac779 https://doi.org/10.1152/ajpheart.1998.274.3.h868

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Pressure-overload hypertrophy is unabated in mice devoid of AT1Areceptors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Pressure-overload hypertrophy is unabated in mice devoid of AT1Areceptors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider