Osmotic effectors in kidneys of xeric and mesic rodents: corticomedullary distributions and changes with water availability.

Urea, sodium, the methylamines glycine betaine and glycerophosphorylcholine (GPC), and the polyols sorbitol and myo-inositol are reported to be the major osmolytes in kidneys of laboratory mammals. These were measured (millimoles per kilogram wet weight) in kidney regions and urines of three species of wild rodents with different dehydration tolerances: the pocket mouse Perognathus parvus (xeric), vole Microtus montanus (mesic), and deer mouse Peromyscus m. gambeli (intermediate). In animals kept without water for 4-6 days, sodium, urea, betaine and GPC + choline were found in gradients increasing from cortex to outer to inner medulla in all species, with Perognathus having the highest levels. Sorbitol was high in the inner medulla but low in the cortex and outer medulla; inositol was highest in the outer medulla. Totals of methylamines and methylamines plus polyols in the medulla showed high linear correlations (positive) with urea and with sodium values. Whole medullae were analyzed at several time points in Microtus and Peromyscus subject to water diuresis followed by antidiuresis. In 102 h diuresis in Microtus, all osmolytes decreased except inositol; however, only urea, sodium and sorbitol reached new steady states within 24 h. Urea returned to initial values in 18 h antidiuresis, while other osmolytes required up to 90 h. In Peromyscus, all osmolytes except the polyols declined in diuresis (max. 78 h test period). During antidiuresis, urea and GPC + choline rose to initial values in 18 h, with sodium and betaine requiring more time. In plots of both species combined, total methylamines + polyols correlated linearly (positive) with sodium, and GPC + choline with urea. Estimates of tissue concentrations suggest that total methylamines + polyols can account for intracellular osmotic balance in all species in antidiuresis and that sufficient concentrations of methylamines may be present to counteract perturbing effects of urea on proteins.