Cooper S J
Life Sci. 1983 May 23;32(21):2453-9. doi: 10.1016/0024-3205(83)90371-5.
Several investigators have shown that anxiolytic benzodiazepines stimulate additional water consumption in rats made thirsty by water deprivation. The present report extends this work by showing that chlordiazepoxide (CDP) enhanced drinking in rats challenged with either cellular or extracellular dehydration, following hypertonic saline or polyethylene glycol injection respectively. Since CDP also increased drinking in control animals, it may have produced a direct dipsogenic effect which acted additively with respect to the physiological thirst challenges. In contrast, CDP did not enhance water intake during the dipsogenic action of the beta-adrenergic agonist, isoproterenol. The data provide new evidence that benzodiazepine mechanisms may be involved in thirst and the controls of drinking.
几位研究人员已表明,抗焦虑苯二氮䓬类药物会刺激因缺水而口渴的大鼠增加饮水量。本报告扩展了这项研究,表明氯氮卓(CDP)分别在注射高渗盐水或聚乙二醇后,增强了受到细胞内或细胞外脱水挑战的大鼠的饮水量。由于CDP也增加了对照动物的饮水量,它可能产生了一种直接的致渴作用,这种作用相对于生理口渴挑战具有累加效应。相比之下,在β-肾上腺素能激动剂异丙肾上腺素的致渴作用期间,CDP并没有增加水的摄入量。这些数据提供了新的证据,表明苯二氮䓬类药物的机制可能参与口渴和饮水控制。