Effect of renal interstitial infusion of L-dopa on sodium and phosphate excretions

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Abstract

It has been hypothesized that dopamine synthesized by the proximal tubule can act as a paracrine substance that regulates reabsorption by the proximal tubule. The present study was performed to study the effects of the stimulation of endogenous synthesis of dopamine by infusion of L-DOPA directly into the renal interstitium on sodium and phosphate excretions and to determine the roles of D1 and D2 receptors in the response. The infusion of L-DOPA (50 µg/kg/min) into the renal interstitium through an implanted matrix significantly increased the fractional excretion of sodium (FENa) from 1.0% ± 0.2% to 3.1% ± 0.6% and the fractional excretion of phosphate (FEPi) from 23% ± 3% to 36% ± 3%, P < .05, n = 10. The infusion of D1 receptor antagonist SCH23390 or SKF83566 (5 µg/kg/min) into the renal interstitium blocked the natriuretic (FENa 1.5% ± 0.2% to 1.9% ± 0.4%) and phosphaturic (FEPi 41% ± 3% to 41% ± 4%) effects of L-DOPA infusion. The infusion of the D2 receptor antagonist sulpiride at a rate of 4 µg/kg/min into the renal interstitium also attenuated the natriuretic (FENa 1.3% ± 0.3% to 1.6% ± 0.5%) and phosphaturic effects of L-DOPA infusion (FEPi 36% ± 5% to 39% ± 5%). We conclude that the renal interstitial infusion of L-DOPA increases sodium and phosphate excretions and that these responses are mediated by D1 and D2 receptors.

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