|
|
||||||||
AJP - Renal Physiology, Vol 260, Issue 5 619-F625, Copyright © 1991 by American Physiological Society
ARTICLES |
J. H. Veis, B. A. Molitoris, I. Teitelbaum, J. A. Mansour and T. Berl
Department of Medicine, University of Colorado School of Medicine, Denver.
Myo-inositol (MI) is involved in the adaptation to hyperosmolality. Its uptake by rat inner medullary collecting duct (RIMCD) cells has not been studied. Compared with cells grown in isotonic media, those grown in hyperosmolality display marked enhancement in [3H]MI uptake [counts/min (cpm).microgram protein-1.2 h-1] from 217 +/- 23 to 718 +/- 64, P less than 0.001. This is mimicked by the supplementation with 300 mM mannitol (638 +/- 59, P less than 0.001) but not by 300 mM urea. The increment in [3H]MI is observed at 37 degrees C but not at 4 degrees C. MI uptake is Na+ dependent in cells grown both in hyperosmolal or isotonic media. At least 12 h of hyperosmolality are needed to enhance MI uptake, and reexposure to isotonic media for at least 24 h is required for the enhancement to reverse. The effects of the microtubular inhibitor, nocodazole (10 micrograms/ml), and the protein synthesis inhibitor, cycloheximide (30 micrograms/ml), were studied. Cells grown with nocodazole show unimpaired enhancement of MI uptake. Cycloheximide exposure (16 h) does not affect MI uptake in isotonic media (182 +/- 23 vs. 191 +/- 15), but inhibited enhanced MI uptake in hyperosmolality (822 +/- 53 in the absence vs. 331 +/- 24 in the presence of cycloheximide, P less than 0.001). We conclude that hyperosmolality stimulates the synthesis of a protein, most likely an Na-MI cotransporter, that markedly enhances MI uptake. This process may be critical to the osmoregulation of RIMCD cells.
This article has been cited by other articles:
![]() |
J. M. Capasso, C. J. Rivard, and T. Berl Silencing and overexpression of the {gamma}-subunit of Na-K-ATPase directly affect survival of IMCD3 cells in response to hypertonic stress Am J Physiol Renal Physiol, December 1, 2006; 291(6): F1142 - F1147. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. M. Capasso, C. J. Rivard, and T. Berl Synthesis of the Na-K-ATPase {gamma}-subunit is regulated at both the transcriptional and translational levels in IMCD3 cells Am J Physiol Renal Physiol, January 1, 2005; 288(1): F76 - F81. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. M. Capasso, C. J. Rivard, and T. Berl Long-term adaptation of renal cells to hypertonicity: role of MAP kinases and Na-K-ATPase Am J Physiol Renal Physiol, May 1, 2001; 280(5): F768 - F776. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. A. Yorek, J. A. Dunlap, W. Liu, and W. L. Lowe Jr. Normalization of hyperosmotic-induced inositol uptake by renal and endothelial cells is regulated by NF-kappa B Am J Physiol Cell Physiol, May 1, 2000; 278(5): C1011 - C1018. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. A. Wojtaszek, L. E. Heasley, G. Siriwardana, and T. Berl Dominant-Negative c-Jun NH2-terminal Kinase 2 Sensitizes Renal Inner Medullary Collecting Duct Cells to Hypertonicity-induced Lethality Independent of Organic Osmolyte Transport J. Biol. Chem., January 9, 1998; 273(2): 800 - 804. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. M. Capasso, C. Rivard, and T. Berl The expression of the gamma subunit of Na-K-ATPase is regulated by osmolality via C-terminal Jun kinase and phosphatidylinositol 3-kinase-dependent mechanisms PNAS, November 6, 2001; 98(23): 13414 - 13419. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |