Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity
Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity
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DOI：
10.1152/ajprenal.00388.2002
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发表时间：
2003-10-01
影响因子：
4.2
通讯作者：
Prewitt, RL
中科院分区：
文献类型：
--
作者：
Dobrian, AD;Schriver, SD;Prewitt, RL
已知高盐饮食在高血压动物模型和人类中诱发或加重高血压。当Sprague-Dawley大鼠（n = 60）被喂食中等高脂肪饮食（32%千卡脂肪，0.8%NaCl）10周时，约一半发展成肥胖[肥胖倾向（OP）]和轻度高血压，而另一半[肥胖抵抗（OR）]保持与低脂对照（C）相当的体重并且血压正常。本研究的目的是测试高氯化钠饮食（2%和4%氯化钠）对高血压和肥胖，氧化应激和肾功能的发展的影响。2%和4% NaCl均能引起OP大鼠早期收缩压升高，而OR和C大鼠则无此作用。高盐摄入诱导的脂肪细胞的大小和数量减少的增加，伴随着循环瘦素在OP大鼠的两倍增加。主动脉超氧化物生成表明OP高盐组与正常盐组相比增加了2.8倍，而尿异前列腺素没有显著增加。此外，在2和4% NaCl的OP大鼠中，肾脏中的羟基壬烯醛蛋白加合物高度增加，表明肾组织中存在氧化应激。与0.8% NaCl相比，2% NaCl组OP的尿白蛋白增加了3倍，4% NaCl组的尿白蛋白增加了4倍。肾脏组织学显示高盐饮食的OP大鼠肾小球硬化程度较高。总之，高盐饮食加速了高血压的发展，但没有增加高血压的严重程度;高盐增加了血管和肾脏的氧化应激，并诱导肾小球硬化和微量白蛋白尿。此外，高盐的OP大鼠显示脂肪细胞肥大和瘦素产生增加。
High-salt diet is known to induce or aggravate hypertension in animal models of hypertension and in humans. When Sprague-Dawley rats (n = 60) are fed a moderately high-fat diet (32% kcal fat, 0.8% NaCl) for 10 wk, about one-half develop obesity [obesity prone (OP)] and mild hypertension, whereas the other half [obesity resistant (OR)] maintain body weight equivalent to a low-fat control (C) and are normotensive. The aim of this study was to test the effect of high-NaCl diets (2 and 4% NaCl) on the development of hypertension and obesity, oxidative stress, and renal function. Both 2 and 4% NaCl induced an early increase in systolic blood pressure of OP but not OR or C rats. High-salt intake induced an increase in the size and reduction in number of adipocytes, concomitant to a twofold increase in circulating leptin in OP rats. Aortic superoxide generation indicated a 2.8-fold increase in the OP high-salt vs. normal-salt groups, whereas urine isoprostanes were not significantly increased. Also, hydroxynonenal protein adducts in the kidney were highly increased in OP rats on 2 and 4% NaCl, indicating oxidative stress in the renal tissue. Urine albumin was increased threefold in the OP on 2% NaCl and fourfold in the same group on 4% NaCl vs. 0.8% NaCl. Kidney histology indicated a higher degree of glomerulosclerosis in OP rats on high-salt diets. In summary, high-salt diet accelerated the development but did not increase the severity of hypertension; high salt increased oxidative stress in the vasculature and kidney and induced kidney glomerulosclerosis and microalbuminuria. Also, the OP rats on high salt displayed adipocyte hypertrophy and increased leptin production.