AJP - Renal Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 254: F165-F177, 1988;
0363-6127/88 $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
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 Kinter, L. B.
Right arrow Articles by Stassen, F. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kinter, L. B.
Right arrow Articles by Stassen, F. L.

AJP - Renal Physiology, Vol 254, Issue 2 165-F177, Copyright © 1988 by American Physiological Society

ARTICLES

Antagonists of the antidiuretic activity of vasopressin

L. B. Kinter, W. F. Huffman and F. L. Stassen
Department of Pharmacology, Smith Kline & French Laboratories, Swedeland, Pennsylvania 19479.

Competitive antagonists of the antidiuretic (ADH) activity of vasopressin were first described some six years ago. When studied in vitro, ADH antagonists displace vasopressin from specific renal binding sites and antagonize, in a competitive fashion, vasopressin stimulation of adenylate cyclase and transepithelial water, salt, and urea fluxes. When studied in vivo, the ADH antagonists increase renal water excretion and antagonize, in a competitive fashion, the ADH activity of vasopressin. Marked species heterogeneity is apparent with ADH antagonists in vivo, and inconsistencies between in vitro and in vivo findings within the same species are reported. Other renal responses associated with administration of ADH antagonists include changes in renal hemodynamics and renal salt and urea excretion. The effects on salt excretion appear to be limited to those species in which vasopressin stimulation of epithelial salt reabsorption has been demonstrated. In summary, the role of vasopressin as the principal factor regulating renal water handling is supported by experience with ADH receptor antagonists. However, that experience also indicates the emerging significance of autocoids, and other synergistic factors, to affect ADH receptor/effector mechanisms and to modulate renal ADH responses.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
R. Musa-Aziz, M. L. M. Barreto-Chaves, and M. De Mello-Aires
Peritubular AVP regulates bicarbonate reabsorption in cortical distal tubule via V1 and V2 receptors
Am J Physiol Renal Physiol, February 1, 2002; 282(2): F256 - F264.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
J. A. Durr, J. Hensen, T. Ehnis, and M. S. Blankenship
Chlorpropamide upregulates antidiuretic hormone receptors and unmasks constitutive receptor signaling
Am J Physiol Renal Physiol, May 1, 2000; 278(5): F799 - F808.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
N. Cotte, M.-N. Balestre, S. Phalipou, M. Hibert, M. Manning, C. Barberis, and B. Mouillac
Identification of Residues Responsible for the Selective Binding of Peptide Antagonists and Agonists in the V2 Vasopressin Receptor
J. Biol. Chem., November 6, 1998; 273(45): 29462 - 29468.
[Abstract] [Full Text] [PDF]


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