Adrenalectomy blocks the compensatory increases in UT-A1 and AQP2 in diabetic rat kidney

The Journal of Membrane Biology
J D KleinJ M Sands


In normal rats we showed that glucocorticoids participate in the downregulation of UT-A1 protein abundance in the inner medullary tip and in lowering of basal and vasopressin-stimulated facilitated urea permeability in terminal IMCDs. To examine the relevance of this response to a rat model of human disease, we studied rats with uncontrolled diabetes mellitus (DM) induced by streptozotocin (STZ), since these rats have increased corticosterone production and urea excretion. We found that at 3 days of DM, UT-A1 protein abundance is downregulated in the inner medullary tip compared to pair-fed control rats, while DM for more than 7 days caused an increase in UT-A1. To test whether adrenal steroids could be a mechanism contributing to the latter increase, we studied adrenalectomized rats (ADX), ADX rats given STZ to induce diabetes (ADX + STZ), and ADX + STZ rats receiving exogenous aldosterone or dexamethasone. In contrast to control rats, UT-A1 protein abundance was not increased by prolonged DM in the ADX rats. Aquaporin 2 (AQP2) was not increased in the inner medullas of 10-day DM rats either. However, UT-A1 protein abundance was significantly reduced in the inner medullary tips from both diabetic aldosterone-treated (40 +/- 2%...Continue Reading


Feb 1, 1990·European Journal of Clinical Investigation·T P AlmdalH Vilstrup
Sep 8, 2001·American Journal of Physiology. Cell Physiology·R T TimmerJ M Sands
Apr 17, 2003·American Journal of Physiology. Renal Physiology·Dongun KimJanet D Klein
Jan 30, 2004·American Journal of Physiology. Cell Physiology·Otto FröhlichRobert B Gunn
Feb 24, 2004·Journal of the American Society of Nephrology : JASN·Randy A GertnerJeff M Sands

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Jun 29, 2010·Lancet·Ning CheungTien Yin Wong

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