We have shown that urea transport across the terminal inner medullary collecting duct (terminal IMCD) is mediated by a vasopressin-stimulated, facilitated diffusion process exhibiting properties consistent with a transporter. To investigate whether hypertonic NaCI, as exists in vivo in the inner medulla, affects urea permeability, we studied isolated perfused rat terminal IMCD segments. Perfusate and bath osmolality were varied symmetrically by adding or removing NaCI or mannitol. Urea permeability rose progressively when osmolality was increased with NaCI or mannitol from 290 to 690 mOsm/kg H20 in the absence of vasopressin; there was no further increase at 890 mOsm/kg H20. In the presence of 10-8 M arginine vasopressin, urea permeability increased when NaCI was added to raise osmolality from 290 to 490 mOsm/kg H20 but there was no further increase at 690 mOsm/kg H20. When 1 mM 8-bromo cyclic AMP was added to the bath, raising NaCI still increased urea permeability. These results suggest that urea transport across the rat terminal IMCD is regulated both by vasopressin and by osmolality at values present in the renal inner medulla. Osmolality seems to activate urea transport across the rat terminal IMCD by mechanisms distinct from those of vasopressin or cyclic AMP. (J. Clin. Invest. 1991.

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Sorbitol production in the renal medulla increases in dehydrated rats, indicating that aldose reductase activity varies with the state of hydration. This response could be due to an increased synthesis of the enzyme (Moriyama T et al. J Biol Chem 1989:264:16810-16814) and/or a change in aldose reductase activity caused by acute changes in intracellular ionic composition, ionic strength, osmolality, or pH. Aldose reductase activity in tubules dissected from kidneys of control rats and rats undergoing water diuresis was measured, and the tubules were permeabilized so that changes in intracellular composition that would occur during dehydration could be induced experimentally. Aldose reductase activity did not change consistently as sodium, potassium, chloride, or osmolality were varied. Aldose reductase activity did increase acutely when sulfate was raised or when pH was lowered to pH 6.2 to 6.8, corresponding to the pH optimum of the enzyme. The small magnitude of change in enzyme activity suggests that the major influence of dehydration on aldose reductase activity is to increase enzyme synthesis. It was concluded that aldose reductase activity is not acutely regulated by changes in sodium, potassium, chloride, or osmolality. The stability of aldose reductase activity despite changes in ionic composition or osmolality supports the hypothesis that acute regulation of intracellular sorbitol content occurs by variation in cell sorbitol permeability and not by variation in cell sorbitol production.