Neurotransmitter mechanisms that mediate the effect of ethanol on urine output were examined in male rats. To establish the neuronal systems involved in the diuretic action of ethanol, urine output was evaluated in animals pretreated with various pharmacological agents. The intraventricular administration of norepinephrine (1.5–12 μg) increased the diuresis produced by a 1.25 g/kg dose of ethanol. Clonidine (2.5, 5.0 μg), an α2‐receptor agonist, also increased ethanol diuresis, while the α1‐raceptor antagonist phentol‐amine (14 and 35 μg) reduced it β1,2‐Adrenergk blocker propranolol (5 and 10 μg) significantly depressed ethanol‐induced urine output Conversely the β2,2‐noradrenergic agonist isoproterenol (5 and 10 μg) increased the diuretic action of ethanol. On the other hand dopamine (4–20 μg) and serotonin (8 and 20 μg) had no effect on ethanol diuresis when given intraventriculariy. These results indicate that the diuretic action of ethanol involves noradrenergic mechanisms.