Pohorecky L A, Packard K
Alcohol Clin Exp Res. 1986 Mar-Apr;10(2):177-83. doi: 10.1111/j.1530-0277.1986.tb05068.x.
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.
在雄性大鼠中研究了介导乙醇对尿量影响的神经递质机制。为了确定参与乙醇利尿作用的神经元系统，对用各种药理剂预处理的动物的尿量进行了评估。脑室内注射去甲肾上腺素（1.5 - 12微克）增加了1.25克/千克剂量乙醇产生的利尿作用。α2受体激动剂可乐定（2.5、5.0微克）也增加了乙醇利尿作用，而α1受体拮抗剂酚妥拉明（14和35微克）则降低了乙醇利尿作用。β1,2肾上腺素能阻滞剂普萘洛尔（5和10微克）显著降低了乙醇诱导的尿量。相反，β2,2去甲肾上腺素能激动剂异丙肾上腺素（5和10微克）增加了乙醇的利尿作用。另一方面，多巴胺（4 - 20微克）和5-羟色胺（8和20微克）脑室内给药时对乙醇利尿作用无影响。这些结果表明乙醇的利尿作用涉及去甲肾上腺素能机制。
