Impaired urinary concentrating ability and cyclic AMP in K+-depleted rat kidney.
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.
D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism*; D004032:Diet; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology*; D007671:Kidney Concentrating Ability; D011191:Potassium Deficiency / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D012964:Sodium / Q000378:metabolism; D014667:Vasopressins / Q000502:physiology
D014667:Vasopressins; D012964:Sodium; D000242:Cyclic AMP