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AJP - Renal Physiology, Vol 267, Issue 1 139-F145, Copyright © 1994 by American Physiological Society
ARTICLES |
T. Nakanishi, Y. Takamitsu, H. Nakahama and M. Sugita
Fifth Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
To determine the relationship between accumulation of osmolytes and maximal urinary concentration in potassium depletion, we tested the effects of experimental water diuresis or potassium depletion on osmolytes in the renal medulla of rats. Hyperosmotic stress was imposed by 4 days of water deprivation for the purpose of establishing the maximal concentrating ability or by the infusion of sodium for the purpose of loading the equal amounts of sodium to the renal medulla. In the diuresis group, water deprivation failed to increase betaine, sorbitol, and taurine contents to the same level as the untreated group, although sodium infusion increased betaine and sorbitol. In the potassium depletion group followed by water deprivation, urine osmolality (2,490 +/- 241 vs. 3,425 +/- 268 mosmol/kgH2O) and all osmolytes were significantly lower than in the untreated group. In response to hyperosmolality with sodium infusion, myo-inositol and glycerophosphorylcholine contents rose to the level of the untreated group. Medullary betaine (67.6 +/- 6.8 vs. 99.5 +/- 8.9), taurine (44.7 +/- 2.4 vs. 61.4 +/- 6.2) and sorbitol (35.6 +/- 4.4 vs. 57.0 +/- 8.4 mmol/kg protein) contents were reduced in potassium-depleted rats when the renal medulla was as hypertonic as in the untreated group. In conclusion, the processing of betaine, taurine, and sorbitol accumulation appeared to be impaired in potassium depletion.
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