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Am J Physiol Heart Circ Physiol 277: H2482-H2487, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 6, H2482-H2487, December 1999

SPECIAL TOPIC
AT1-receptor blockade enhances ischemic preconditioning in hypertrophied rat myocardium

Karyn L. Butler1,2, Alice H. Huang2, and Judith K. Gwathmey3

Departments of 1 Surgery and 2 Physiology, Morehouse School of Medicine, Atlanta, Georgia 30310; and 3 Departments of Medicine and Physiology, Boston University School of Medicine, Boston, Massachusetts 02138

The purpose of this study was to determine whether ischemic preconditioning protects contractile function in hypertrophied rat myocardium from ischemia-reperfusion (I/R) injury. Male salt-sensitive rats were fed a high-salt diet for 2 wk to induce myocardial hypertrophy. Nonhypertrophied hearts were obtained from age-matched Sprague-Dawley (SD) rats fed a regular diet. Heart weight-to-body weight ratios were higher in salt-sensitive rats than in SD rats (6.9 ± 0.2 vs. 4.7 ± 0.2 g/kg, P < 0.01). A second group of salt-sensitive and SD rats was administered losartan (10 mg · kg-1 · day-1), an AT1-receptor blocker, for 1 wk before the study. Isolated hearts were preconditioned with transient ischemia before global I/R. After I/R, preconditioned hypertrophied hearts exhibited greater recovery of left ventricular developed pressure compared with that of preconditioned normal hearts (73 ± 8 vs. 18 ± 8%, P < 0.01). Left ventricular developed pressure was further enhanced by losartan in both hypertrophied and normal myocardium (99 ± 5 vs. 73 ± 8%, P < 0.05 and 97 ± 15 vs. 18 ± 8%, P < 0.01). Hypertrophied rat myocardium can be protected from I/R-induced contractile dysfunction by ischemic preconditioning. Losartan improves the ischemic tolerance of normal and hypertrophied myocardium.

angiotensin II receptors; cardiac preconditioning; myocardial hypertrophy


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