Hirsch D J, Hirtle R W
Can J Physiol Pharmacol. 1986 Sep;64(9):1170-6. doi: 10.1139/y86-199.
The mechanism of impaired water excretion in adrenalectomized mammals is unclear. Previous workers have suggested that one cause might be increased water permeability of the distal nephron, allowing back diffusion of water from tubular fluid diluted by the ascending limb. Evidence to support this mechanism in previous studies has been confounded by simultaneous changes in steroid and antidiuretic hormone levels. We compared osmotic and diffusional water permeability of the surface late distal tubule in vivo in intact and adrenalectomized Brattleboro rats, which are free of antidiuretic hormone. The adrenalectomized rats were demonstrated to have impaired diluting capacity in clearance studies. Adrenalectomized rats had a sixfold increase in osmotic permeability and a 1.5-fold increase in diffusional permeability over intact controls. Adrenal steroids have a specific action on water permeability of the distal nephron, independent of antidiuretic hormone.
肾上腺切除的哺乳动物水排泄受损的机制尚不清楚。以前的研究人员认为,一个原因可能是远端肾单位水通透性增加,使得被升支稀释的肾小管液中的水发生逆向扩散。以往研究中支持这一机制的证据因类固醇和抗利尿激素水平的同时变化而混淆。我们比较了完整的和肾上腺切除的Brattleboro大鼠(缺乏抗利尿激素)体内表面晚期远端小管的渗透水通透性和扩散水通透性。在清除率研究中,肾上腺切除的大鼠表现出稀释能力受损。与完整对照组相比,肾上腺切除的大鼠渗透通透性增加了6倍,扩散通透性增加了1.5倍。肾上腺类固醇对远端肾单位的水通透性有特定作用,独立于抗利尿激素。