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Vasopressin increases urea permeability in the initial IMCD from diabetic rats

Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia

Submitted 30 March 2005 ; accepted in final form 7 May 2005

In normal rats, vasopressin and hyperosmolality enhance urea permeability (P_urea) in the terminal, but not in the initial inner medullary collecting duct (IMCD), a process thought to occur through the UT-A1 urea transporter. In the terminal IMCD, UT-A1 is detected as 97- and 117-kDa glycoproteins. However, in the initial IMCD, only the 97-kDa form is detected. During streptozotocin-induced diabetes mellitus, UT-A1 protein abundance is increased, and the 117-kDa UT-A1 glycoprotein appears in the initial IMCD. We hypothesize that the 117-kDa glycoprotein mediates the vasopressin- and osmolality-induced changes in P_urea. Thus, in the present study, we measured P_urea in in vitro perfused initial IMCDs from diabetic rats by imposing a 5 mM bath-to-lumen urea gradient without any osmotic gradient. Basal P_urea was similar in control vs. diabetic rats (3 ± 1 vs. 5 ± 1 x 10^–5 cm/s, n = 4, P = not significant). Vasopressin (10 nM) significantly increased P_urea to 16 ± 5 x 10^–5 cm/s (n = 4, P < 0.05) in diabetic but not in control rats. Forskolin (10 µM, adenylyl cyclase activator) also significantly increased P_urea in diabetic rats. In contrast, increasing osmolality to 690 mosmol/kgH₂O did not change P_urea in diabetic rats. We conclude that initial IMCDs from diabetic rats have vasopressin- and forskolin-, but not hyperosmolality-stimulated P_urea. The appearance of vasopressin-stimulated P_urea in initial IMCDs correlates with an increase in UT-A1 protein abundance and the appearance of the 117-kDa UT-A1 glycoprotein in this region during diabetes. This suggests that the 117-kDa UT-A1 glycoprotein is necessary for vasopressin-stimulated urea transport.

diabetes mellitus; inner medullary collecting duct; hyperosmolality

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