|
|
||||||||
AJP - Renal Physiology, Vol 269, Issue 1 70-F77, Copyright © 1995 by American Physiological Society
ARTICLES |
C. L. Chou, S. R. DiGiovanni, R. Mejia, S. Nielsen and M. A. Knepper
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Circulating concentrations of oxytocin increase to 10-40 pM in rats in response to osmotic stimuli, suggesting that oxytocin could play a role in regulation of water balance. The present studies tested whether oxytocin at such concentrations increases osmotic water permeability (Pf) in isolated perfused terminal inner medullary collecting ducts (IMCD). In IMCD segments from Sprague-Dawley rats, 20 pM oxytocin added to the peritubular bath caused a two- to threefold increase in Pf, whereas 200 pM oxytocin increased Pf by five- to sixfold (n = 8, P < 0.01). IMCD from Brattleboro rats, which manifest central diabetes insipidus, exhibited a 2.8-fold increase in Pf in response to 20 pM oxytocin and a 4.7-fold increase in response to 200 pM oxytocin. However, in Brattleboro rats, the response to 20 pM oxytocin was dependent on prior water restriction of the rats. Immunoblotting showed no change in the expression of the aquaporin-CD water channel in Brattleboro rats in response to water restriction. Nevertheless, immunofluorescence studies of inner medullary tissue from Brattleboro rats revealed a marked redistribution of the aquaporin-CD water channels to a predominantly apical and subapical localization in IMCD cells in response to water restriction, similar to the redistribution seen in response to vasopressin. Mathematical modeling studies revealed that the measured increase in Pf in response to oxytocin is sufficient to generate a concentrated urine. We conclude that oxytocin can function physiologically as an antidiuretic hormone, mimicking the short-term action of vasopressin on water permeability, albeit with somewhat lower potency.
This article has been cited by other articles:
![]() |
K.-P. Yip Epac-mediated Ca2+ mobilization and exocytosis in inner medullary collecting duct Am J Physiol Renal Physiol, October 1, 2006; 291(4): F882 - F890. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. M. Christensen, W. Wang, J. Frokiar, and S. Nielsen Axial heterogeneity in basolateral AQP2 localization in rat kidney: effect of vasopressin Am J Physiol Renal Physiol, April 1, 2003; 284(4): F701 - F717. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Nielsen, J. Frokiar, D. Marples, T.-H. Kwon, P. Agre, and M. A. Knepper Aquaporins in the Kidney: From Molecules to Medicine Physiol Rev, January 1, 2002; 82(1): 205 - 244. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Pouzet, C. Serradeil-Le Gal, N. Bouby, J.-P. Maffrand, G. Le Fur, and L. Bankir Selective blockade of vasopressin V2 receptors reveals significant V2-mediated water reabsorption in Brattleboro rats with diabetes insipidus Nephrol. Dial. Transplant., April 1, 2001; 16(4): 725 - 734. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Promeneur, T.-H. Kwon, J. Frokiar, M. A. Knepper, and S. Nielsen Vasopressin V2-receptor-dependent regulation of AQP2 expression in Brattleboro rats Am J Physiol Renal Physiol, August 1, 2000; 279(2): F370 - F382. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. S. Weinstein, S. Yu, and C. A. Ecelbarger Variable imprinting of the heterotrimeric G protein Gs alpha -subunit within different segments of the nephron Am J Physiol Renal Physiol, April 1, 2000; 278(4): F507 - F514. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. M. Christensen, M. Zelenina, A. Aperia, and S. Nielsen Localization and regulation of PKA-phosphorylated AQP2 in response to V2-receptor agonist/antagonist treatment Am J Physiol Renal Physiol, January 1, 2000; 278(1): F29 - F42. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |