T. Nakanishi et al., IMPAIRMENT OF RENAL MEDULLARY OSMOLYTE ACCUMULATION IN POTASSIUM-DEPLETED RATS, The American journal of physiology, 267(1), 1994, pp. 60000139-60000145
To determine the relationship between accumulation of osmolytes and ma
ximal urinary concentration in potassium depletion, we tested the effe
cts of experimental water diuresis or potassium depletion on osmolytes
in the renal medulla of rats. Hyperosmotic stress was imposed by 4 da
ys of water deprivation for the purpose of establishing the maximal co
ncentrating ability or by the infusion of sodium for the purpose of lo
ading the equal amounts of sodium to the renal medulla. In the diuresi
s group, water deprivation failed to increase betaine, sorbitol, and t
aurine contents to the same level as the untreated group, although sod
ium infusion increased betaine and sorbitol. In the potassium depletio
n group followed by water deprivation, urine osmolality (2,490 +/- 241
vs. 3,425 +/- 268 mosmol/kgH(2)O) and all osmolytes were significantl
y lower than in the untreated group. In response to hyperosmolality wi
th 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 so
rbitol (35.6 +/- 4.4 vs. 57.0 +/- 8.4 mmol/kg protein) contents were r
educed in potassium-depleted rats when the renal medulla was as hypert
onic as in the untreated group. In conclusion, the processing of betai
ne, taurine, and sorbitol accumulation appeared to be impaired in pota
ssium depletion.