Preferential release of renal dopamine into the tubule lumen: effect of chronic sodium loading

Dopamine (DA), produced by the renal proximal tubule, has been demonstrated as an intrarenal paracrine hormone mediating diuresis and natriuresis. The precise mechanism by which DA exerts its cell-to-cell action is not fully understood. In the present study, renal interstitial (RIF) DA (by in vivo microdialysis) and urinary DA excretion (UDAV) were compared in anesthetized rats on either normal (0.28% NaCl, NS) or high (4.0% NaCl, HS) sodium balance (n = 9 in each group). Urine flow (UV) and sodium excretion (UNaV) in HS were greater than in NS rats (UV 7.2 +/- 0.6 vs 3.8 +/- 0.3 microliters/min, P < 0.01; UNaV 497 +/- 66 vs 265 +/- 27 nmol/min, P < 0.01). In rats on both NS and HS balance, UDAV was significantly higher than RIF DA (420 +/- 37 vs 3.68 +/- 0.49 pg/min in the NS rat; 601 +/- 68 vs 1.25 +/- 0.36 pg/min in the HS rat, both P < 0.01). UDAV was increased in HS compared with NS rats (601 +/- 68 vs 420 +/- 37 pg/min, P < 0.05). In contrast, RIF DA was significantly lower in HS than NS rats (1.25 +/- 0.36 vs 3.68 +/- 0.49 pg/min, P < 0.01). In conclusion, chronic sodium loading increased renal DA production and release predominantly into the tubular lumen rather than the peritubular interstitial space of the kidney. These results indicate that DA originating from proximal tubule cells has a direct tubule action in the control of sodium excretion.