INTERACTION OF HYPERTENSION AND CALORIC RESTRICTION ON CARDIAC MASS AND ISOMYOSIN EXPRESSION

被引:24
作者
SWOAP, SJ [1 ]
BODDELL, P [1 ]
BALDWIN, KM [1 ]
机构
[1] UNIV CALIF IRVINE, DEPT PHYSIOL & BIOPHYS, IRVINE, CA 92717 USA
关键词
BLOOD PRESSURE; MYOSIN HEAVY CHAIN; HEART; CARDIAC MUSCLE; PLASTICITY; FOOD RESTRICTION;
D O I
10.1152/ajpregu.1995.268.1.R33
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Previous studies show that elevations in blood pressure induce concomitant increases in both cardiac mass and slow beta-myosin heavy chain (MHC) expression in rodents, whereas caloric restriction of 50% (CR) causes an increase in beta-MHC while modestly lowering blood pressure in normotensive rats. The goals of this study were to 1) determine if beta-MHC expression could be independently regulated by CR and hypertension when these two interventions are combined and 2) determine if CR exerts a lowering of blood pressure in two contrasting models of rodent hypertension. Rodents were assigned to the following groups: 1) normal control (NC); 2) abdominal aortic constriction (Abcon), a model that induces hypertension via renin-angiotensin II; 3) nephrectomy-deoxycorticosterone acetate treatment (DOCA), a model that induces hypertension through increased salt retention; 4) CR; 5) Abcon+CR; 6) DOCA+CR. Results show that both Abcon and DOCA induced significant increases in systemic blood pressures, left ventricular (LV) weight/body weight, and the relative content of beta-MHC compared with NC. When applied in combination with either Abcon or DOCA, CR significantly blunted the changes observed in both systemic blood pressures and LV weight/body weight. In contrast, CR in conjunction with DOCA augmented %beta-MHC expression relative to either DOCA or CR alone. These data suggest 1) caloric restriction exerts a powerful impact on reducing experimentally induced hypertension in rodents and 2) the regulation of beta-MHC expression appears to be regulated by at least two processes, one associated with the stimulus of hypertension and the other involving an independent pathway linked to caloric restriction.
引用
收藏
页码:R33 / R39
页数:7
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