Noradrenergic mechanisms in ethanol diuresis.

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 micrograms) increased the diuresis produced by a 1.25 g/kg dose of ethanol. Clonidine (2.5, 5.0 micrograms), an alpha 2-receptor agonist, also increased ethanol diuresis, while the alpha 1-receptor antagonist phentolamine (14 and 35 micrograms) reduced it. beta 1,2-Adrenergic blocker propranolol (5 and 10 micrograms) significantly depressed ethanol-induced urine output. Conversely the beta 2,2-noradrenergic agonist isoproterenol (5 and 10 micrograms) increased the diuretic action of ethanol. On the other hand dopamine (4-20 micrograms) and serotonin (8 and 20 micrograms) had no effect on ethanol diuresis when given intraventricularly. These results indicate that the diuretic action of ethanol involves noradrenergic mechanisms.