1 The probable involvement of dopamine in the regulation of water excretion was investigated by administering dopamine antagonists intravenously to barbiturate -anaesthetized rats undergoing a water diuresis induced by the infusion of 0.83% glucose with 0.3% NaCl at the rate of 9 ml h-'. 2 Administration of 100l ig of the D,-/D2-dopamine antagonist, haloperidol, reduced the enhanced urine flow of rats infused with the hypotonic solution by 69% (from 75.4 ± 13.0 to 23.6 ± 6.0 pI min-', P<0.01). Similarly, the D,-receptor antagonist, SCH23390, reduced urine flow by 58% (from 77.5 ± 9.2 to 32.7 ± 7.2p fmin-', P <0.01) and the D2-receptor antagonist, sulpiride, by 47% (from 66.2 ± 8.6 to 35.1 ± 6.8 pidmin-', P < 0.05).3 The injection of SCH 23390 increased the urine osmolality from 189.6 ± 27.5 to 479.8 ± 45.8 mosm kg-' (P < 0.05). There was no significant change in sodium and potassium excretion in any of the experiments. Blood pressure (BP) decreased after haloperidol and SCH 23390 injection from control values of 121.7 ± 1.7 and 116.5 ± 7.4 to 113.3 ± 3.3 and 106.0 ± 8.8 mmHg respectively (P < 0.05). 4 To study whether the influence of dopamine antagonists on urine flow during water diuresis depends on antidiuretic hormone (ADH), we administered 0.6 Ag d(CH2)5-D-Phe-Ile-AVP (an ADH antagonist) shortly after the injection of l00 g SCH 23390. The preferential V2 ADH-antagonist abolished the antidiuretic effect of SCH 23390 but did not affect its blood pressure reducing effect (from 118.6 ± 5.6 to 103.2 ± 4.6 mmHg, P <0.01). 5 These results suggest that dopamine antagonists blunted the hypotonic saline-induced diuresis by favouring ADH release through an interference with an inhibitory dopaminergic pathway.