| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Renal Division, Department of Medcine, Emory University, Atlanta, GA, USA; Department of Physiology, Emory University School of Medicine, Atlanta, GA, USA
2 Renal Division, Department of Medcine, Emory University, Atlanta, GA, USA
3 Renal Division, Department of Medcine, Emory University, Atlanta, GA, USA; Department of Pediatrics, The Catholic University of Korea, Seoul, Republic of Korea
* To whom correspondence should be addressed. E-mail: jeff.sands{at}emory.edu.
Rats with diabetes mellitus have an increase in UT-A1 urea transporter protein abundance and absolute urea excretion, but the relative amount (percent) of urea in total urinary solute is actually decreased due to the marked glucosuria. Urea-specific signaling pathways have been identified in mIMCD3 cells and renal medulla, suggesting the possibility that changes in the percentage or concentration of urea could be a factor that regulates UT-A1 abundance. In this study, we tested the hypothesis that an increase of a urinary solute other than urea would increase UT-A1 abundance, similar to diabetes mellitus, while an increase in urine urea would not. In both inner medullary base and tip, UT-A1 protein abundance increased during NaCl or glucose-induced osmotic diuresis, but not during urea-induced osmotic diuresis. Next, rats undergoing NaCl or glucose diuresis were given supplemental urea to increase the percentage of urine urea to control values. UT-A1 abundance did not increase in these urea-supplemented rats, compared to control rats. Additionally, both UT-A2 and UT-B protein abundances in the outer medulla increased during urea-induced osmotic diuresis, but not in NaCl or glucose diuresis. We conclude that during osmotic diuresis: UT-A1 abundance increases when the percentage of urea in total urinary solute is low; and UT-A2 and UT-B abundances increase when the urea concentration in the medullary interstitium is high. These findings suggest that a reduction in urine or interstitial urea results in an increase in UT-A1 protein abundance in an attempt to restore inner medullary interstitial urea and preserve urine concentrating ability.
This article has been cited by other articles:
|
|
 |
|
  M. S. Kwon, S. W. Lim, and H. M. Kwon Hypertonic Stress in the Kidney: A Necessary Evil Physiology, June 1, 2009; 24(3): 186 - 191. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-M. Kim, W.-Y. Kim, H.-W. Lee, J. Kim, H. M. Kwon, J. D. Klein, J. M. Sands, and D. Kim Urea and NaCl regulate UT-A1 urea transporter in opposing directions via TonEBP pathway during osmotic diuresis Am J Physiol Renal Physiol, January 1, 2009; 296(1): F67 - F77. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. D. Klein, B. P. Murrell, S. Tucker, Y.-H. Kim, and J. M. Sands Urea transporter UT-A1 and aquaporin-2 proteins decrease in response to angiotensin II or norepinephrine-induced acute hypertension Am J Physiol Renal Physiol, November 1, 2006; 291(5): F952 - F959. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. D. Klein, O. Frohlich, M. A. Blount, C. F. Martin, T. D. Smith, and J. M. Sands Vasopressin Increases Plasma Membrane Accumulation of Urea Transporter UT-A1 in Rat Inner Medullary Collecting Ducts J. Am. Soc. Nephrol., October 1, 2006; 17(10): 2680 - 2686. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Inoue, S. D. Kozlowski, J. D. Klein, J. L. Bailey, J. M. Sands, and S. M. Bagnasco Regulated expression of renal and intestinal UT-B urea transporter in response to varying urea load Am J Physiol Renal Physiol, August 1, 2005; 289(2): F451 - F458. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Xu, W. Tian, J. N. Lindsley, T. T. Oyama, J. M. Capasso, C. J. Rivard, H. T. Cohen, S. M. Bagnasco, S. Anderson, and D. M. Cohen EphA2: expression in the renal medulla and regulation by hypertonicity and urea stress in vitro and in vivo Am J Physiol Renal Physiol, April 1, 2005; 288(4): F855 - F866. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
