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June 1, 1994AJP Heart and Circulatory Physiology163 citations

ANG II receptor blockade prevents ventricular hypertrophy and ANF gene expression with pressure overload in mice

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HRH. A. RockmanSWS. P. WachhorstLML. Mao

Key Result

AT1 receptor blockade with losartan prevented the increase in heart weight-to-body weight ratio in mice with pressure overload compared to untreated controls (0.506 vs 0.634 g/g x 100, P<0.0001).

Structured PICO

Does losartan or captopril prevent cardiac hypertrophy in adult mice subjected to left ventricular pressure overload?

P
Population
Adult mice subjected to left ventricular pressure overload by transverse aortic constriction (TAC) (n=56) and sham-operated controls (n=21), total n=77
I
Intervention
Losartan (1.05 g/l) or captopril (2 g/l) administered in drinking water for 7 days
C
Comparator
No treatment administered in drinking water
O
Outcome
Heart weight-to-body weight ratiosurrogate

Angiotensin II receptor blockade and ACE inhibition prevent or attenuate cardiac hypertrophy induced by pressure overload in mice, independent of hemodynamic load.

Main Result

Absolute Event Rate: 0.506% vs 0.634%

p-value: p=<0.0001

Abstract

There is increasing evidence that the renin-angiotensin system may play a important role in cardiac hypertrophy. To assess the role of angiotensin II in the induction of cardiac hypertrophy, three groups of adult mice were subjected to left ventricular pressure overload by transverse aortic constriction (TAC). For the next 7 days the groups received either the specific angiotensin II subtype 1 receptor (AT1) antagonist (losartan, 1.05 g/l; n = 17), an angiotensin enzyme inhibitor (captopril, 2 g/l; n = 17), or no treatment (n = 22) administered in the drinking water and compared with three similarly treated sham-operated groups (n = 7 each). TAC resulted in a significant increase in heart weight-to-body weight ratio (0.634 +/- 0.087 vs. 0.525 +/- 0.039, g/g x 100, P < 0.05), which was prevented by losartan (0.506 +/- 0.069, g/g x 100, P < 0.0001) despite similar hemodynamic load (proximal systolic pressure 146 +/- 31 vs. 136 +/- 32 mmHg, untreated vs. losartan, P = NS). Proximal systolic pressure was positively correlated with the development of ventricular hypertrophy. In the presence of AT1-receptor blockade, the increase in heart weight-to-body weight ratio at any given systolic pressure was significantly attenuated compared with untreated TAC mice. The increase in heart weight-to-body weight ratio was also significantly attenuated by captopril compared with untreated banded controls (0.542 +/- 0.091, g/g x 100, P = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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Cite This Study

Rockman et al. (1994) studied Left ventricular pressure overload / cardiac hypertrophy (n=77). Losartan or Captopril vs. No treatment and sham operation was evaluated on Heart weight-to-body weight ratio (g/g x 100) (p=<0.0001). AT1 receptor blockade with losartan prevented the increase in heart weight-to-body weight ratio in mice with pressure overload compared to untreated controls (0.506 vs 0.634 g/g x 100, P<0.0001).

synapsesocial.com/papers/6a0dda6be51d8d6d0c09dc46https://doi.org/10.1152/ajpheart.1994.266.6.h2468
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