Ernsberger P, Koletsky R J, Baskin J S, Foley M
Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio 44106.
Hypertension. 1994 Dec;24(6):699-705. doi: 10.1161/01.hyp.24.6.699.
Very-low-calorie diets lower blood pressure acutely in obese humans and rats. However, refeeding after dietary restriction produces mild hypertension in rats. Refeeding hypertension was characterized in genetically obese spontaneously hypertensive rats (obese SHR, Koletsky rat), a model of genetic obesity and hypertension. Obese SHR were fed a restricted diet (Optifast) for 12 days, refed ad libitum for 28 days, dieted again for 12 days, and then refed 4 days and killed. Control obese SHR and lean SHR littermates were fed ad libitum continuously. Dietary restriction led to rapid weight loss followed by prompt regain to baseline weight after return to unrestricted food intake. Heart rate fell with institution of the low-calorie diet and returned to baseline on refeeding. Blood pressure became elevated during refeeding in dieted obese SHR relative to ad libitum fed obese SHR controls. The fall in blood pressure after ganglionic blockade with chlorisondamine was exaggerated in refed obese SHR, and cardiac beta-adrenergic receptors were downregulated. Both of these findings imply increased sympathetic tone. The left ventricular wall was thicker in the refed obese SHR than in the ad libitum fed obese SHR. Shorter cycles of weight loss and regain in lean SHR led to transient increases in blood pressure and heart rate. Cycles of dietary restriction and refeeding in obese SHR elicit sustained blood pressure elevation via sympathetic activation and exacerbate cardiac hypertrophy. Drastic fluctuations in nutrient intake may not be advantageous in hypertension.
极低热量饮食可使肥胖人类和大鼠的血压迅速降低。然而,饮食限制后的再喂养会使大鼠出现轻度高血压。在遗传性肥胖自发性高血压大鼠(肥胖型SHR,科莱茨基大鼠)中对再喂养高血压进行了研究,该大鼠是遗传性肥胖和高血压的模型。给肥胖型SHR喂食限制饮食(Optifast)12天,自由进食28天,再次节食12天,然后再喂养4天并处死。对照肥胖型SHR和瘦型SHR同窝仔鼠持续自由进食。饮食限制导致体重迅速下降,恢复无限制食物摄入后体重迅速恢复到基线水平。随着低热量饮食的开始,心率下降,再喂养时恢复到基线水平。与自由进食的肥胖型SHR对照相比,节食的肥胖型SHR在再喂养期间血压升高。在用氯异吲哚胺进行神经节阻断后,再喂养的肥胖型SHR血压下降更为明显,且心脏β-肾上腺素能受体下调。这两个发现都表明交感神经张力增加。再喂养的肥胖型SHR的左心室壁比自由进食的肥胖型SHR更厚。瘦型SHR体重减轻和恢复的周期较短会导致血压和心率短暂升高。肥胖型SHR的饮食限制和再喂养周期通过交感神经激活引起持续的血压升高,并加剧心脏肥大。营养摄入的剧烈波动对高血压可能并无益处。