Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 257: C612-C620, 1989;
0363-6143/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Blazer-Yost, B. L.
Right arrow Articles by Furlanetto, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Blazer-Yost, B. L.
Right arrow Articles by Furlanetto, R.

AJP - Cell Physiology, Vol 257, Issue 4 C612-C620, Copyright © 1989 by American Physiological Society

ARTICLES

Insulin and IGF I receptor-mediated Na+ transport in toad urinary bladders

B. L. Blazer-Yost, M. Cox and R. Furlanetto
Department of Medicine, Veterans Administration Medical Center, Philadelphia, Pennsylvania.

We compared the concentration dependence of insulin- and insulin-like growth factor I (IGF I)-stimulated Na+ transport with ligand-receptor affinities in the urinary bladder of the toad Bufo marinus. Threshold, half-maximal, and maximal natriferic concentrations of both peptides were approximately 0.1, 1, and 10 nM, respectively. Amiloride, but not ethyl isopropyl amiloride, (10(-5) M), abolished Na+ transport. Maximal responses to either peptide rendered the tissue insensitive to challenge with the other. Separate insulin and IGF I receptors were identified by equilibrium binding and polyacrylamide gel electrophoresis of cross-linked ligand-receptor complexes. For both peptides, half-maximal binding occurred at 3-10 nM; crossover binding to the other receptor occurred with 10- and 100-fold lower affinity. Thus, in this model "high-resistance" renal epithelium, 1) ligand binding to specific insulin and IGF I receptors stimulates transcellular Na+ flux, 2) the natriferic effects of insulin and IGF I apparently depend on activation of apical Na+ channels rather than Na+-H+ antiporters, and 3) the natriferic pathways activated by insulin and IGF I appear to converge subsequent to ligand-receptor binding but before the final transport ("effector") step(s).


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
A. Taruno, N. Niisato, and Y. Marunaka
Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases
Am J Physiol Renal Physiol, July 1, 2007; 293(1): F128 - F138.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
B. L. Blazer-Yost, J. C. Vahle, J. M. Byars, and R. L. Bacallao
Real-time three-dimensional imaging of lipid signal transduction: apical membrane insertion of epithelial Na+ channels
Am J Physiol Cell Physiol, December 1, 2004; 287(6): C1569 - C1576.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
Y. Wei, Y.-J. Chen, D. Li, R. Gu, and W.-H. Wang
Dual effect of insulin-like growth factor on the apical 70-pS K channel in the thick ascending limb of rat kidney
Am J Physiol Cell Physiol, June 1, 2004; 286(6): C1258 - C1263.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
N. Y. Tallini and L. C. Stoner
Amiloride-sensitive sodium current in everted Ambystoma initial collecting tubule: short-term insulin effects
Am J Physiol Cell Physiol, October 1, 2002; 283(4): C1171 - C1181.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
B. L. Blazer-Yost, X. Liu, and S. I. Helman
Hormonal regulation of ENaCs: insulin and aldosterone
Am J Physiol Cell Physiol, May 1, 1998; 274(5): C1373 - C1379.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online