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1 Department of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: thussain2{at}uh.edu.
Angiotensin II AT2 receptors have been implicated to play a role in the regulation of renal/cardiovascular functions under pathological conditions. The present study is designed to investigate the function of the AT2 receptors on renal sodium excretion and the AT2 receptor expression in the cortical membranes of streptozotocin (STZ) induced diabetic rats. The STZ treatment led to a significant weight loss, hyperglycemia, and decrease in plasma insulin levels comparing with control rats. STZ-induced diabetic rats had significantly elevated basal UF, UNaV, FENa, and urinary cGMP comparing with control rats. Infusion of PD123319, an AT2 receptor antagonist, caused a significant decrease in UNaV (µmole/min) in STZ-induced diabetic rats (1±0.09 vs. 0.45±0.1) but not in control rats (0.35±10.05 vs. 0.4 ±0.07). The decrease in UNaV was associated with a significant decrease in urinary cGMP levels (pmole/min) in STZ-induced diabetic rats (21±2 vs. 10±0.8) but not in control rats (11.75±3 vs. 12.6±2). The infusion of PD123319 did not alter GFR (STZ: 0.3±0.02 vs. 0.25±0.03; control: 1.4±0.05 vs. 1.5±0.09 ml/min) or MAP (STZ: 82±3 vs. 79±3.5; control: 90±4 vs. 89±4 mmHg) suggesting a tubular effect of the drug. Western blot analysis using AT2 receptor antibody revealed a significantly enhanced expression of the AT2 receptor protein (~45kDa) in brushborder (~50 folds) and basolateral membranes (~80 folds) of STZ-induced diabetic comparing with control rats. In conclusion, our data suggest that the tubular AT2 receptors in diabetic rats are profoundly enhanced and possibly via a cGMP pathway promote sodium excretion in this model of diabetes.
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