Key result
Caloric restriction significantly blunted the increases in systemic blood pressure and left ventricular weight induced by experimental hypertension models in rodents.
Why the study?
Does caloric restriction reduce blood pressure and alter cardiac mass and beta-MHC expression in rodent models of hypertension?
Does caloric restriction reduce blood pressure and alter cardiac mass and beta-MHC expression in rodent models of hypertension?
Caloric restriction blunts experimentally induced hypertension and cardiac hypertrophy in rodents while independently regulating beta-MHC expression.
Answers are grounded in this paper and cite their sources.
Does not support caloric restriction for human hypertension; leaves open translation of rodent findings to clinical practice.
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.
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Swoap et al. (1995) studied hypertension. Caloric restriction (CR) vs. Normal control, Abcon alone, DOCA alone was evaluated on Systemic blood pressures, left ventricular (LV) weight/body weight, and relative content of beta-MHC. Caloric restriction significantly blunted the increases in systemic blood pressure and left ventricular weight induced by experimental hypertension models in rodents.
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