AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 257: H1110-H1118, 1989;
0363-6135/89 $5.00
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AJP - Heart and Circulatory Physiology, Vol 257, Issue 4 1110-H1118, Copyright © 1989 by American Physiological Society


ARTICLES

Role of lowering arterial pressure on maximal coronary flow with and without regression of cardiac hypertrophy

C. A. Canby and R. J. Tomanek
Department of Anatomy, University of Iowa, Iowa City 52242.

This study was initiated to test the hypothesis that attenuation of long-term hypertension with or without regression of left ventricular hypertrophy (LVH) will lower minimal coronary vascular resistance (MCVR). Six-month-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with captopril or hydralazine for a period of 3 mo. Myocardial perfusion, measured with microspheres, and hemodynamic data were obtained in awake, unrestrained rats aged 9 mo. MCVR was calculated from the quotient of mean/myocardial perfusion. Both drugs significantly lowered arterial systolic pressure in both strains of rats, but only captopril was effective in reducing heart mass. Left ventricular MCVR per 100 g was lower in captopril-treated WKY (0.064 +/- 0.012) and SHR (0.079 +/- 0.006) than the untreated controls (SHR: 0.124 +/- 0.006; WKY: 0.098 +/- 0.009), whereas total LV MCVR was unaltered by treatment. Hydralazine tended to lower LV MCVR per 100 g in both strains despite its tendency to increase ventricular mass. Captopril, but not hydralazine, treatment was associated with a significant increase in capillary density in both WKY and SHR. We conclude that the improvement in MCVR is related to both the regression of LVH and to the consequences of lowering arterial systolic pressure. In contrast, the increase in capillary density appears to be related to the decrease in ventricular mass after captopril treatment.


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