Noradrenergic Mechanisms in Ethanol Diuresis

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Abstract
Neurotransmitter mechanisms that mediate the effect of ethanol on urine output were examined in male rats. To establish the neuronal systems invovled in the diurectic action of ethanol, urine output was evaluated in animals pretreated with various pharmacological agents. The intraventricular administration of norepinephrine (1.5-12 .mu.g) increased the diuresis produced by a 1.25 g/kg dose of ethanol. Clonidine (2.5, 5.0 .mu.g), an .alpha.2-receptor agonist, also increased ethanol diuresis, while the .alpha.1-receptor antagonist phentolamine (14 and 35 .mu.g) reduced it. .beta.1,2-Adrenegic blocker propranolol (5 and 10 .mu.g) significantly depressed ethanol-induced urine output. Conversely the .beta.2,2-noradrenegic agonist isoproterenol (5 and 10 .mu.g) increased the diuretic action of ethanol. On the other hand dopamine (4-20 .mu.g) and serotonin (8 and 20 .mu.g) had no effect on ethanol diuresis when given intraventricularly. These results indicate that the diurectic action of ethanol involves noradrenergic mechanisms.