高血压和热量限制对心脏质量和异肌球蛋白表达的相互作用。

S. Swoap, P. Boddell, K. Baldwin
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引用次数: 14

摘要

先前的研究表明,血压升高会导致啮齿动物心脏质量和慢速β -肌球蛋白重链(MHC)表达的增加,而热量限制50% (CR)会导致β -MHC的增加,同时适度降低血压。本研究的目的是:1)确定当CR和高血压联合干预时,β - mhc的表达是否可以独立调节;2)确定CR是否在两种对比的啮齿动物高血压模型中起到降低血压的作用。随机分为:1)正常对照组(NC);2)腹主动脉收缩(Abcon),肾素-血管紧张素II诱导高血压模型;3)肾切除术联合醋酸脱氧皮质酮治疗(DOCA),这是一种通过增加盐潴留诱导高血压的模型;4)铬;5) Abcon + CR;6) DOCA + CR。结果显示,与NC相比,Abcon和DOCA均能显著升高全身血压、左室(LV)重量/体重以及β - mhc的相对含量。当与Abcon或DOCA联合应用时,CR显着减弱了体血压和左室体重/体重的变化。相比之下,与DOCA或CR单独相比,CR联合DOCA可增强% β - mhc表达。这些数据表明:1)热量限制对降低实验性诱导的啮齿动物高血压具有强大的影响;2)β - mhc表达的调节似乎受到至少两个过程的调节,一个与高血压刺激有关,另一个涉及与热量限制相关的独立途径。
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Interaction of hypertension and caloric restriction on cardiac mass and isomyosin expression.
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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