The interaction between renal nerves, endothelins acting via endothelin-A receptors and vasopressin in the regulation of renal excretory function was investigated. In conscious intact and renal denervated diabetes insipidus (DI) Brattleboro rats, as well as their controls, Long-Evans (LE) rats, an infusion of 16.4 nmol/kg/min ET<sub>A</sub> receptor antagonist BQ-123 was performed in the course of 50 min. Femoral artery blood pressure, heart rate, C<sub>cr</sub>, V · U<sub>Na</sub>, V · U<sub>K</sub> and V · U<sub>Cl</sub> did not alter in any of the groups. Urine flow rate diminished by 38.1% (p < 0.02), while urine osmolality increased by 30.3% (p < 0.05) as a result of BQ-123 infusion in the intact LE rats but neither urine flow rate nor urine osmolality changed in the DI rats. In contrast to intact LE rats, BQ-123 infusion in renal denervated LE rats did not alter urine flow rate or urine osmolality. However, urine flow rate in renal denervated DI rats surprisingly decreased by 71.1% (p < 0.01) while urine osmolality increased by 161% (p < 0.001) as a result of BQ-123 infusion. Endogenous endothelins can regulate renal water excretion through ET<sub>A</sub> receptor activation. Renal sympathetic nerves participate in the modulation of renal water excretion influencing the ET<sub>A</sub> receptor-mediated effects of endothelins in the kidney.