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Reduced renal dopamine D₁ receptor function in streptozotocin-induced diabetic rats

Heart and Kidney Institute, College of Pharmacy, University of Houston, Houston, Texas 77204

Submitted 20 June 2003 ; accepted in final form 4 November 2003

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 fourfold increase in plasma levels of glucose along with a significant decrease in insulin levels compared with control rats. Intravenous administration of SKF-38393, a D₁ receptor agonist, caused a threefold 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 with control rats. Moreover, SKF-38393 failed to stimulate GTPS binding in proximal tubular membranes from diabetic rats compared with control rats. We conclude that the natriuretic response to D₁ receptor activation is reduced in type I diabetes as a result of a decrease in D₁ receptor expression and defective receptor G protein coupling. These abnormalities may contribute to the sodium retention associated with type I diabetes.

G proteins; hyperglycemia; Na-K-ATPase; natriuresis; SKF-38393

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