Key result
Imidapril significantly improved sarcoplasmic reticulum Ca2+-ATPase activity (54.2 vs 40.5 p moles Pi/cell/hour, p<0.01) and prevented myocardial hypertrophy in hypertensive rats.
Why the study?
Does imidapril prevent left ventricular remodeling and metabolic dysfunction of myocardial organelles in spontaneously hypertensive rats compared to diltiazem or vehicle?
Population
40 10-week-old male spontaneously hypertensive rats and 20 10-week-old male normotensive Wistar-Kyoto rats
Comparison
Imidapril 2.5 mg/kg per day or diltiazem 30… vs Vehicle administered orally via stomach tube…
Design
Preclinical, randomly divided into three groups of 10 animals
Follow-up
8 weeks
Authors
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Hypothesis-generating for ACE inhibition in hypertensive LV remodeling; should not yet change clinical practice.
Does imidapril prevent left ventricular remodeling and metabolic dysfunction of myocardial organelles in spontaneously hypertensive rats compared to diltiazem or vehicle?
Absolute Event Rate: 54.2% vs 40.5%
p-value: p=<0.01
ACE inhibition with imidapril prevents hypertension-induced left ventricular remodeling and counteracts early metabolic dysfunction of myocardial organelles in spontaneously hypertensive rats better than calcium-channel blockade with diltiazem.
Watanabe et al. (1997) studied Hypertension (Spontaneously Hypertensive Rats) (n=60). Imidapril vs. Vehicle or Diltiazem (30 mg/kg per day) was evaluated on Sarcoplasmic reticulum Ca2+-ATPase activity (p moles Pi/cell/hour) (p=<0.01). Imidapril significantly improved sarcoplasmic reticulum Ca2+-ATPase activity (54.2 vs 40.5 p moles Pi/cell/hour, p<0.01) and prevented myocardial hypertrophy in hypertensive rats.
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