What is the clinical evidence from this study?

Study design: Other. Population: Hypertension (n=53). Intervention: Delapril vs. Vehicle (5% arabic gum). Primary outcome: Left ventricular weight (therapeutic protocol) (p=<0.05).

January 1, 2000Open Access

Non-Corresponding Effects of an Angiotensin-Converting Enzyme Inhibitor on Cardiac and Vascular Hypertrophy in Spontaneously Hypertensive Rats.

Q: What are the key findings of this study?

Delapril significantly reduced left ventricular weight compared to control (64 vs 69 mg/100 g body weight, p<0.05) in spontaneously hypertensive rats, but did not reduce vascular hypertrophy.

MTMasahiko TozawaThird Way STShuichi TakishitaKagoshima University HMHiromi MurataniKyushu Sangyo University

Key Result

Delapril significantly reduced left ventricular weight compared to control (64 vs 69 mg/100 g body weight, p<0.05) in spontaneously hypertensive rats, but did not reduce vascular hypertrophy.

Structured PICO

Does delapril reduce cardiac and vascular hypertrophy in spontaneously hypertensive rats?

Population

53 male spontaneously hypertensive rats were treated with delapril or vehicle in preventive or therapeutic protocols to assess effects on cardiac and vascular hypertrophy.

Intervention

Delapril (ACEI) 30 mg/kg/day administered in a preventive (4 to 28 weeks of age) or a therapeutic (12-24 weeks of age) protocol

Comparator

Vehicle (5% arabic gum)

Outcome

Hypertrophy of the heart and hypertrophy of the coronary and renal interlobular arteriessurrogate

Delapril reduces cardiac hypertrophy but not coronary and renal artery hypertrophy in spontaneously hypertensive rats, with arginine vasopressin potentially playing a role in cardiac hypertrophy etiology.

Main Result

Absolute Event Rate: 64% vs 69%

p-value: p=<0.05

Limitations

Animal model (SHR) may not fully translate to human hypertension
Use of 1% NaCl in drinking water made hypertension relatively refractory to ACEI administration, resulting in only mild blood pressure reduction

Abstract

Angiotensin-converting enzyme inhibitors (ACEIs) may have different effects on cardiac hypertrophy than on vascular hypertrophy. Arginine vasopressin (AVP) may promote cardiac hypertrophy. Our aims were (1) to simultaneously examine the chronic effects of ACEIs on hypertrophy of the heart and hypertrophy of the coronary and renal interlobular arteries, and (2) to clarify the relation between AVP concentration (AVPC) and cardiac hypertrophy. ACEI (delapril: 30 mg/kg/day) or vehicle (5% arabic gum) was administered in a preventive (4 to 28 weeks of age) or a therapeutic (12-24 weeks of age) protocol in spontaneously hypertensive rats. In both protocols, delapril produced a slight but significant decrease in systolic blood pressure. In the therapeutic protocol, the weight of the left ventricle (mean+/-SE) was lower (p<0.05) in the ACEI group (64+/-2 mg/100 g body weight) than in the control group (69+/-1 mg/100 g body weight). Plasma renin activity was significantly higher in the ACEI group than in the control group in both the preventive (p <0.01) and therapeutic (p<0.01) protocols. In the therapeutic protocol, AVPC was significantly (p<0.05) lower in the ACEI group than in the control group. AVPC was significantly (p=0.02, r=0.46) correlated with the weight of the left ventricle in the therapeutic protocol. For both protocols, no differences were noted between the ACEI and control groups in the vascular hypertrophy of the coronary and renal interlobular arteries. We conclude that (1) the preventive or therapeutic effect of ACEIs on hypertrophy may not be the same in the heart as in the coronary and renal arteries; and (2) AVP was significantly correlated with the left ventricular weight. This indicates that AVP could play a role in the etiology of cardiac hypertrophy in SHR.

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