Intrarenal dopamine participation in frusemide diuretic and natriuretic responses to frusemide

1. Dopamine (DA) involvement in the renal response to frusemide was analysed using the isolated perfused rat kidney preparation. Endogenous DA levels were increased through the infusion of its precursor levodopa (LD) (0.5 or 1 microM) whereas benserazide (50 or 100 microM), an inhibitor of the enzyme L-dopa-decarboxylase, was used to decrease DA synthesis. 2. Frusemide administration (0.3-20 nmols) induced a dose-dependent increase in fractional excretion of water (FE H2O), sodium (FE Na+) and glucose (FEG). FE Na+ elicited by the diuretic was enhanced 30-40% by 0.5 microM of LD (n = 5, P < 0.05), and 60-80% by LD 1 microM (n = 5, P < 0.05). FE H2O produced by the diuretic was enlarged 80-100% by 0.5 microM (n = 5, P = 0.05), and 130-170% by 1 microM of LD (n = 5, P < 0.01). The increase produced by both concentrations of LD on FEG was 200% for the lowest dose of the diuretic (n = 5, P < 0.01), and 90% for the highest (n = 5, P < 0.05). 3. Benserazide (BZ) (100 microM) decreased the F.E. Na+ induced by frusemide (n = 5, P < 0.05) by 32-42%, and completely abolished frusemide effects on FE H2O and FEG (n = 5). 4. In conclusion, our results suggest that endogenous dopamine participates in the frusemide-induced diuresis and sodium excretion within the kidney, and that the participation of extrarenal factors is not essential for this effect. Dopamine may be involved in frusemide-induced inhibition of proximal sodium reabsorption.