Dawson R, Liu S, Jung B, Messina S, Eppler B
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville 32610, USA.
Amino Acids. 2000;19(3-4):643-65. doi: 10.1007/s007260070014.
Taurine is present in high concentrations in mammalian tissues and has been implicated in cardiovascular control mechanisms. The aim of the present study was to evaluate the ability of taurine to attenuate salt-induced elevations in blood pressure and markers of damage to the kidney and cardiovascular system in stroke prone spontaneously hypertensive rats (SPSHR). Male SPSHR (6 weeks old) were placed on high salt diets that contained 1% (w/w) NaCl added to their normal chow for 84 days and then were switched to 3% added NaCl for the remaining 63 days of the study. SPSHR was given 1.5% taurine in the drinking water (n = 8), a taurine free diet (n = 8) or normal chow (n = 8). A final control group (n = 6) was not given high salt diets. High salt diets caused an acceleration in the development of hypertension in all groups. Taurine supplementation reduced ventricular hypertrophy and decreased urinary excretion of protein and creatinine. The taurine free diet did not alter serum or urinary excretion of taurine, but did result in elevated urinary nitrogen excretion, increased serum cholesterol levels, and impaired performance in a spatial learning task. Alterations in dietary taurine intake did not alter urinary or serum electrolytes (Na+, K+), but taurine supplementation did attenuate a rise in serum calcium seen with the high salt diets. Urinary excretion (microg/24h) of epinephrine and dopamine was significantly reduced in SPSHR given 1% NaCl in the diet, but this effect was not seen in SPSHR on taurine free or supplemented diets. Taurine supplementation showed cardioprotective and renoprotective effects in SPSHR given high salt diets.
牛磺酸在哺乳动物组织中含量很高,并与心血管控制机制有关。本研究的目的是评估牛磺酸减轻盐诱导的易中风自发性高血压大鼠(SPSHR)血压升高以及肾脏和心血管系统损伤标志物的能力。雄性SPSHR(6周龄)被置于高盐饮食中,在其正常食物中添加1%(w/w)NaCl,持续84天,然后在研究的剩余63天切换到添加3%NaCl的饮食。给SPSHR饮用含1.5%牛磺酸的水(n = 8)、无牛磺酸饮食(n = 8)或正常食物(n = 8)。最后一个对照组(n = 6)未给予高盐饮食。高盐饮食导致所有组的高血压发展加速。补充牛磺酸可减轻心室肥厚,并减少蛋白质和肌酐的尿排泄。无牛磺酸饮食并未改变牛磺酸的血清或尿排泄,但确实导致尿氮排泄增加、血清胆固醇水平升高以及空间学习任务表现受损。饮食中牛磺酸摄入量的改变并未改变尿或血清电解质(Na+、K+),但补充牛磺酸确实减轻了高盐饮食时出现的血清钙升高。饮食中添加1%NaCl的SPSHR肾上腺素和多巴胺的尿排泄(μg/24小时)显著降低,但在无牛磺酸或补充牛磺酸饮食的SPSHR中未观察到这种效应。在给予高盐饮食的SPSHR中,补充牛磺酸显示出心脏保护和肾脏保护作用。