Dobrian Anca D, Schriver Suzanne D, Lynch Terrie, Prewitt Russell L
Department of Physiological Sciences, Eastern Virginia Medical School, 700W Olney Rd, Norfolk, VA 23507, USA.
Am J Physiol Renal Physiol. 2003 Oct;285(4):F619-28. doi: 10.1152/ajprenal.00388.2002. Epub 2003 Jun 10.
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.
已知高盐饮食会在高血压动物模型和人类中诱发或加重高血压。当给60只斯普拉格-道利大鼠喂食适度高脂肪饮食（32%千卡脂肪，0.8%氯化钠）10周时，约一半大鼠会出现肥胖[肥胖倾向（OP）]和轻度高血压，而另一半[肥胖抵抗（OR）]大鼠体重维持在与低脂对照组（C）相当的水平且血压正常。本研究的目的是测试高氯化钠饮食（2%和4%氯化钠）对高血压和肥胖发展、氧化应激及肾功能的影响。2%和4%氯化钠均使OP大鼠的收缩压早期升高，但对OR大鼠或C大鼠无此影响。高盐摄入导致OP大鼠脂肪细胞大小增加、数量减少，同时循环瘦素增加两倍。主动脉超氧化物生成显示，OP高盐组与正常盐组相比增加了2.8倍，而尿异前列腺素未显著增加。此外，2%和4%氯化钠喂养的OP大鼠肾脏中的羟基壬烯醛蛋白加合物大幅增加，表明肾组织存在氧化应激。与0.8%氯化钠相比，2%氯化钠喂养的OP大鼠尿白蛋白增加了三倍，4%氯化钠喂养的同一组大鼠尿白蛋白增加了四倍。肾脏组织学检查表明，高盐饮食的OP大鼠肾小球硬化程度更高。总之，高盐饮食加速了高血压的发展，但未增加其严重程度；高盐增加了血管和肾脏的氧化应激，导致肾小球硬化和微量白蛋白尿。此外，高盐喂养的OP大鼠出现脂肪细胞肥大和瘦素分泌增加。
