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

Citation
Sj. Swoap et al., INTERACTION OF HYPERTENSION AND CALORIC RESTRICTION ON CARDIAC MASS AND ISOMYOSIN EXPRESSION, American journal of physiology. Regulatory, integrative and comparative physiology, 37(1), 1995, pp. 33-39
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
37
Issue
1
Year of publication
1995
Pages
33 - 39
Database
ISI
SICI code
0363-6119(1995)37:1<33:IOHACR>2.0.ZU;2-M
Abstract
Previous studies show that elevations in blood pressure induce concomi tant increases in both cardiac mass and slow beta-myosin heavy chain ( MHC) expression in rodents, whereas caloric restriction of 50% (CR) ca uses an increase in beta-MHC while modestly lowering blood pressure in normotensive rats. The goals of this study were to 1) determine if be ta-MHC expression could be independently regulated by CR and hypertens ion when these two interventions are combined and 2) determine if CR e xerts a lowering of blood pressure in two contrasting models of rodent hypertension. Rodents were assigned to the following groups: 1) norma l control (NC); 2) abdominal aortic constriction (Abcon), a model that induces hypertension via renin-angiotensin II; 3) nephrectomy-deoxyco rticosterone acetate treatment (DOCA), a model that induces hypertensi on through increased salt retention; 4) CR; 5) Abcon+CR; 6) DOCA+CR. R esults show that both Abcon and DOCA induced significant increases in systemic blood pressures, left ventricular (LV) weight/body weight, an d the relative content of beta-MHC compared with NC. When applied in c ombination with either Abcon or DOCA, CR significantly blunted the cha nges observed in both systemic blood pressures and LV weight/body weig ht. In contrast, CR in conjunction with DOCA augmented %beta-MHC expre ssion relative to either DOCA or CR alone. These data suggest 1) calor ic restriction exerts a powerful impact on reducing experimentally ind uced hypertension in rodents and 2) the regulation of beta-MHC express ion appears to be regulated by at least two processes, one associated with the stimulus of hypertension and the other involving an independe nt pathway linked to caloric restriction.