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
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.