Christensen S
Pflugers Arch. 1983 Feb;396(2):106-9. doi: 10.1007/BF00615513.
Male and female Long Evan rats and Brattleboro rats with ADH-deficient diabetes insipidus were treated with lithium administered in the diet for 12 weeks. The plasma lithium level was about 1 mmol/l in all groups. Lithium caused polydipsia and polyuria and lowering of renal concentrating ability in normal rats. In rats with ADH deficiency lithium tended to increase water intake, but did not influence spontaneous urine osmolality or maximal urine osmolality during water deprivation. The results indicate that the renal concentrating defect caused by lithium in rats can be explained by ADH-blockade as the only mechanism. However, there is circumstantial evidence that lithium in addition may stimulate thirst mechanisms by an ADH-independent action.
将雄性和雌性长 Evans 大鼠以及患有抗利尿激素缺乏性尿崩症的 Brattleboro 大鼠,通过在饮食中添加锂进行为期 12 周的处理。所有组的血浆锂水平约为 1 mmol/L。锂可导致正常大鼠出现多饮、多尿以及肾浓缩能力降低。在抗利尿激素缺乏的大鼠中,锂倾向于增加水摄入量,但不影响禁水期间的自发尿渗透压或最大尿渗透压。结果表明,锂在大鼠中引起的肾浓缩缺陷可仅通过抗利尿激素阻断这一机制来解释。然而,有间接证据表明,锂此外可能通过一种不依赖抗利尿激素的作用刺激口渴机制。