Beck N, Webster S K
Am J Physiol. 1976 Oct;231(4):1204-8. doi: 10.1152/ajplegacy.1976.231.4.1204.
The possibility that an alteration of the vasopressin-dependent cyclic AMP system plays a pathogenic role in the urinary concentrating defect in K+ depletion was investigated in the rat. The antidiuretic response to vasopressin was significantly less in K+-depleted rats. In these K+-depleted rats, the increase in urinary cyclic AMP excretion in response to vasopressin was also significantly less. However, repletion of K+ for 1 wk by feeding high-K+ diets restored the ability to increase urinary cyclic AMP excretion in response to vasopressin. In the in vitro incubation of renal medullary slices, the increase in cyclic AMP concentration in response to vasopressin was also significantly less in the slices obtained from K+-depleted rats than in those obtained from control rats. These findings suggest that, in K+ depletion, there is a reversible impairment of the vasopressin-dependent cyclic AMP system in the renal medulla; this impairment may play a pathogenic role in the urinary concentrating defect in K+ depletion.
在大鼠中研究了血管加压素依赖性环磷酸腺苷（cAMP）系统的改变在钾缺乏时尿浓缩功能缺陷中是否起致病作用。钾缺乏的大鼠对血管加压素的抗利尿反应明显较弱。在这些钾缺乏的大鼠中，血管加压素引起的尿中cAMP排泄增加也明显较少。然而，通过喂食高钾饮食补充钾1周后，对血管加压素产生反应增加尿中cAMP排泄的能力得以恢复。在肾髓质切片的体外孵育中，从钾缺乏大鼠获得的切片中，血管加压素引起的cAMP浓度增加也明显低于从对照大鼠获得的切片。这些发现表明，在钾缺乏时，肾髓质中血管加压素依赖性cAMP系统存在可逆性损害；这种损害可能在钾缺乏时的尿浓缩功能缺陷中起致病作用。
