Additional salutary effects of the combination of exercise training and an angiotensin-converting enzyme inhibitor on the left ventricular function of spontaneously hypertensive rats

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Abstract

Objectives

To investigate whether the combination of exercise training with the angiotensin-converting enzyme inhibitor lisinopril will have an additional beneficial effect on left ventricular function in spontaneously hypertensive rats.

Design

Twelve-week-old male rats were assigned to treadmill running (Ht-Ex; 20 m/min at 5° grade, 1 h/day, 5 days/week), or lisinopril treatment (Ht-Lis; 15 mg/kg per day by gavage), or treadmill running while treated with lisinopril (Ht-ExLis), and were compared with a sedentary group (Ht-Sed). Age-matched and sex-matched Wistar-Kyoto rats were controls.

Methods

After 10 weeks of experimentation, left ventricular morphology and function were assessed from M-mode echocardiograms and transmitral Doppler spectra [early (E) and atrial peak velocities (A), their ratio (E/A), and E-wave deceleration time (Edec time) and slope (Edec slope)].

Results

Ht-Sed exhibited prominent concentric left ventricular hypertrophy with systolic and diastolic dysfunctions evidenced by a significantly reduced fractional shortening (%FS) and ‘pseudonormalization’ of left ventricular filling, characterized by an apparently normal E/A ratio despite an underlying left ventricular relaxation abnormality. Exercise training did not significantly alter left ventricular morphology or function. Lisinopril alone attenuated left ventricular hypertrophy and enhanced diastolic function but had no significant effect on systolic function. Combining exercise training with lisinopril treatment increased %FS by 25%, decreased the E/A ratio and Edec slope by 35% and 37%, respectively, and increased Edec time by 82%.

Conclusion

Our results provide experimental evidence that lisinopril administration, when combined with moderate exercise training, is more promising in attenuating cardiac dysfunction than either agent alone in hypertension of a genetic origin.

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