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1 Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA, USA
* To whom correspondence should be addressed. E-mail: dobriaad{at}evms.edu.
High salt diet is known to induce or aggravate hypertension in animal models of hypertension and humans. When Sprague-Dawley rats (n=60) are fed a moderately high fat diet (32kcal% fat, 0.8%NaCl) for 10 weeks, about half develop obesity (obesity-prone, OP) and mild hypertension, whereas the other half (obesity-resistant, OR) maintains 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 the 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 2-fold 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, while 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 3-fold in the OP on 2% NaCl and 4-fold 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.
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