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

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 D-1 and D-2 receptors in the response. The infusion of L-DOPA (50 mu g/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 D-1 receptor antagonist SCH23390 or SKF83566 (5 mu g/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 D-2 receptor antagonist sulpiride ata rate of 4 mu g/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 D-1 and D-2 receptors.