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1 Heart and Kidney Institute, College of Pharmacy, University of Houston, Houston, Texas, USA
* To whom correspondence should be addressed. E-mail: mlokhandwala{at}uh.edu.
Dopamine via activation of renal D1 receptors inhibits the activities of Na,K -ATPase and Na/H exchanger and subsequently increases sodium excretion. Decreased renal dopamine production and sodium excretion are associated with type I diabetes. However, it is not known whether the response to D1 receptor activation is altered in type I diabetes. The present study was designed to examine the effect of streptozotocin-induced type I diabetes on renal D1 receptor expression and function. Streptozotocin treatment of Sprague Dawley rats caused a 4-fold increase in plasma levels of glucose along with significant decrease in insulin levels compared to control rats. Intravenous administration of SKF 38393, a D1 receptor agonist caused a 3-fold increase in sodium excretion in control rats; however, SKF 38393 failed to produce natriuresis in diabetic rats. SKF 38393 caused a concentration dependent inhibition of Na,K-ATPase activity in renal proximal tubules of control rats. However, the ability of SKF 38393 to inhibit Na,K-ATPase activity was markedly diminished in diabetic rats. D1 receptor numbers and protein abundance as determined by [3H]SCH 23390-ligand binding and western blot analysis were markedly reduced in diabetic rats compared to control rats. Moreover, SKF 38393 failed to stimulate GTP
S binding in proximal tubular membranes from diabetic rats compared to control rats. We conclude that the natriuretic response to D1 receptor activation is reduced in type I diabetes as a result of decrease in D1 receptor expression and a defective receptor G-protein coupling. These abnormalities may contribute to the sodium retention associated with type I diabetes.
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