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Am J Physiol Renal Physiol (April 5, 2005). doi:10.1152/ajprenal.00335.2004
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Submitted on September 9, 2004
Accepted on March 22, 2005

Regulation of the Renal Thiazide-Sensitive Na-Cl Cotransporter, Blood Pressure, and Natriuresis in Obese Zucker Rats Treated with Rosiglitazone

Osman Khan1, Shahla Riazi1, Xinqun Hu1, Jian Song1, James B. Wade2, and Carolyn A. Ecelbarger1*

1 Department of Medicine, Division of Endocrinology and Metabolism, Georgetown University, Washington, DC, USA
2 Department of Physiology, University of Maryland, Baltimore, MD, USA

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

Previously, we showed an increase in protein abundance of the renal thiazide-sensitive Na-Cl cotransporter (NCC) in young, pre-diabetic, obese Zucker rats, relative to lean age-mates. To test whether this increase correlated to increased thiazide-sensitivity (NCC activity) and blood pressure, and could be modified by insulin-sensitizing agents, we treated lean and obese Zucker rats (9-weeks old) with either control diet or this diet supplemented with 3 mg/kg.bw rosiglitazone (RGZ), a PPAR-{gamma} agonist and potent insulin-sensitizing agent for 12 weeks (n = 9/group). The rise in blood pressure, measured continuously by radiotelemetry, was significantly blunted in the RGZ-treated obese rats. Similarly, blood glucose and urinary albumin were markedly decreased in these rats. RGZ-treated rats whether lean or obese, excreted a NaCl load faster, but excreted less sodium in response to hydrochlorothiazide, applied as a novel in vivo measure NCC activity. Obese rats had increased renal protein abundance and urinary excretion of NCC, however, this was not significantly reduced by RGZ (densitometry in cortex homogenate - % lean control): 100 ± 9, 93 ± 4, 124 ± 9, and 141 ± 14 for lean control, lean RGZ, obese control, and obese RGZ, respectively. Subcellular localization, as evaluated by confocal microscopy and immunoblotting following differential centrifugation, of NCC was not different between rat groups. Overall, RGZ reduced blood pressure and thiazide-sensitivity, however, the mechanism(s) did not seem to involve a decrease in NCC protein abundance or cellular location. Decreased NCC activity may have contributed to the maintenance of normotension in RGZ-treated obese rats.




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