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1 Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Ga, USA
2 Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Ga, USA; Department of Physiology, Emory University School of Medicine, Atlanta, GA, USA
* To whom correspondence should be addressed. E-mail: jklei01{at}emory.edu.
In rats with streptozotocin-induced diabetes mellitus for 10-20 days, we showed that the abundance of the major medullary transport proteins involved in the urine concentrating mechanism, UT-A1, aquaporin-2 (AQP2), and the Na+-K+-2C- cotransporter (NKCC2/BSC1), are increased, despite the ongoing osmotic diuresis. To test whether vasopressin is necessary for these diabetes mellitus-induced changes in UT-A1, AQP2, or NKCC2/BSC1, we studied Brattleboro rats since they lack vasopressin. Brattleboro rats were given vasopressin (2.4 µg/day via osmotic mini-pump) for 5 or 12 days. At 5 days, vasopressin increased AQP2 protein abundance but decreased UT-A1 abundance, compared to untreated Brattleboro rats. At 12 days, vasopressin increased the abundance of both UT-A1 and AQP2 proteins, but did not alter NKCC2/BSC1. Next, untreated Brattleboro rats were made diabetic for 10 days by injecting them with streptozotocin (40mg/kg). Diabetes mellitus increased the abundance of AQP2 and NKCC2/BSC1 proteins, but UT-A1 protein abundance did not increase. Third, vasopressintreated Brattleboro rats were made diabetic with streptozotocin for 10 days. In vasopressintreated Brattleboro rats, diabetes mellitus increased UT-A1, AQP2, and NKCC2/BSC1 protein abundances. Vasopressin significantly increased UT-A1 phosphorylation in vasopressin-treated diabetic Brattleboro rats, but not in the other groups of Brattleboro rats. We conclude that: [1] administering vasopressin to Brattleboro rats for 12 days, but not for 5 days, increases UT-A1 protein abundance; and [2] vasopressin is necessary for the increase in UT-A1 protein in diabetic rats, but is not necessary for the increase in AQP2 or NKCC2 proteins.
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