help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
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
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Richardson, S. B.
Right arrow Articles by Gibson, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Richardson, S. B.
Right arrow Articles by Gibson, M.

Endocrinology, Vol 126, 1047-1052, Copyright © 1990 by Endocrine Society

ARTICLES

Effects of vasopressin on insulin secretion and inositol phosphate production in a hamster beta cell line (HIT)

SB Richardson, N Eyler, S Twente, M Monaco, N Altszuler and M Gibson
Department of Medicine, VA Medical Center, New York, NY 10010.

The recent isolation of vasopressin (VP) from the rat and human pancreas led us to investigate the effects of VP on insulin secretion. In the SV 40-transformed hamster beta cell line (HIT), 0.1-1.0 nM VP caused rapid stimulation of insulin secretion. Slight but significant inhibition of insulin secretion was observed in the presence of 10 pM VP. These effects of VP on insulin secretion were paralleled by dose- dependent changes in inositol phosphate (IP) production, indicating mediation by V1-type VP receptors. VP stimulated IP3 production at 30 sec and production of IP1 by 60 sec. VP (0.1 nM to 1 microM) failed to stimulate the release or cellular content of cAMP, whereas forskolin was an effective stimulus. Forskolin and VP together caused at least additive stimulation of insulin secretion. Taken together, these observations indicate that VP is not acting via V2-mediated pathways. However, VP-induced stimulation of insulin and IP production were only slightly inhibited by a V1a pressor antagonist in 100- or 1,000-fold excess, indicating that VP effects are not mediated by V1a receptors. The V1 receptor involved may represent a V1b or a novel type of VP receptor. These observations suggest a potential physiological role of VP in regulating insulin secretion.


This article has been cited by other articles:


Home page
 J. Histochem. Cytochem.Home page
H. Kobayashi, S. Nomura, T. Mitsui, T. Ito, N. Kuno, Y. Ohno, K. Kadomatsu, T. Muramatsu, T. Nagasaka, and S. Mizutani
Tissue Distribution of Placental Leucine Aminopeptidase/Oxytocinase During Mouse Pregnancy
J. Histochem. Cytochem., January 1, 2004; 52(1): 113 - 122.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
V. Folny, D. Raufaste, L. Lukovic, B. Pouzet, P. Rochard, M. Pascal, and C. Serradeil-Le Gal
Pancreatic vasopressin V1b receptors: characterization in In-R1-G9 cells and localization in human pancreas
Am J Physiol Endocrinol Metab, September 1, 2003; 285(3): E566 - E576.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1990 by The Endocrine Society