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Am J Physiol Renal Physiol (August 10, 2004). doi:10.1152/ajprenal.00063.2004
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Submitted on February 24, 2004
Accepted on August 4, 2004

Effects of Dietary Fat, NaCl, and Fructose on Renal Sodium and Water Transporter Abundances and Systemic Blood Pressure

Jian Song1, Xinqun Hu1, Min Shi1, Mark A. Knepper2, and Carolyn A. Ecelbarger1*

1 Department of Medicine, Division of Endocrinology and Metabolism, Georgetown University, Washington, DC, USA
2 National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA

* To whom correspondence should be addressed. E-mail: ecelbarc{at}georgetown.edu.

Dietary fructose, NaCl, and/or saturated fat have been correlated with mean arterial pressure (MAP) rises in sensitive strains of rats. Dysregulation of sodium and/or water reabsorption by the kidney may contribute. Utilizing radiotelemetry and parallel semi-quantitative immunoblotting, we examined the effects of various diets on MAP and the regulation of abundance of the major renal sodium and water transport proteins in male, Sprague-Dawley rats. In Study 1, rats (~275 g) were fed 1 of 4 diets for 4 weeks (n = 6/group): 1) control, 2) 65% fructose, 3) control + added NaCl (2.59%), or 4) fructose + NaCl. In Study 2, 5% butter (fat) was added to the above 4 diets. Both fat and NaCl, but not fructose, caused modest rises in MAP (5-10 mm Hg) and increased day-to-night ratio in diastolic blood pressure. NaCl or fructose increased kidney size. Creatinine clearance (CCl) was increased by salt or fat and, fractional excretion of sodium was decreased by fat. In Study 1, high NaCl markedly reduced plasma renin and aldosterone and its regulated proteins in whole kidney, i.e., the thiazide-sensitive Na-Cl cotransporter (NCC) and the {alpha}- and {gamma}- (70-kDa band) subunits of the epithelial sodium channel (ENaC). These effects were blunted by fat. Fructose increased the abundance of the sodium phosphate cotransporter, while it decreased the bumetanide-sensitive Na-K-2Cl cotransporter and aquaporin-2. Overall, doubling of dietary fat appeared to impair dietary sodium adaptation, i.e., blunt the down-regulation of aldosterone-mediated effects, thus allowing blood pressure to rise at an accelerated rate.




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