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


     

Am J Physiol Regul Integr Comp Physiol 272: R1371-R1378, 1997;
0363-6119/97 $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 Karlsson, S.
Right arrow Articles by Ahren, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Karlsson, S.
Right arrow Articles by Ahren, B.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 272, Issue 5 1371-R1378, Copyright © 1997 by American Physiological Society

ARTICLES

Presynaptic sympathetic mechanism in the insulinostatic effect of epinephrine in mouse pancreatic islets

S. Karlsson, U. Myrsen, A. Nieuwenhuizen, F. Sundler and B. Ahren
Department of Medicine, University Hospital of Malmo, Lund University, Sweden.

The catecholamines inhibit insulin release. It is not established whether presynaptic mechanisms contribute to this effect. We therefore examined the relative contribution of presynaptic and postsynaptic mechanisms to the insulinostatic effects of epinephrine and norepinephrine. Mice were injected with 6-hydroxydopamine (6-OHDA; 0.19 mmol/kg) or its vehicle. Islets were isolated after 48 h. Islets from vehicle-injected control animals contained numerous tyrosine hydroxylase (TH)-immunoreactive nerve terminals (marker for sympathetic nerves). In contrast, TH-immunoreactive nerves were not detected in islets from 6-OHDA-treated animals, indicating sympathetic denervation. Basal (5.6 mmol/l glucose) or glucose-stimulated (16.7 mmol/l) insulin secretion did not differ between incubated islets from vehicle-injected control animals and islets from 6-OHDA-treated animals. The insulinostatic effect of epinephrine, but not that of norepinephrine, was markedly impaired in islets from 6-OHDA-treated animals: the lowest effective insulinostatic concentration of epinephrine was 0.01 nmol/l in islets from vehicle-injected animals and 1 nmol/l in islets from 6-OHDA-treated animals. We conclude that in isolated mouse islets the insulinostatic effect of epinephrine, but not that of norepinephrine, partially depends on sympathetic nerve terminals, suggesting an important role for presynaptic mechanisms in epinephrine-induced inhibition of insulin secretion.


This article has been cited by other articles:


Home page
 DiabetesHome page
K. Filipsson, M. Kvist-Reimer, and B. Ahren
The Neuropeptide Pituitary Adenylate Cyclase-Activating Polypeptide and Islet Function
Diabetes, September 1, 2001; 50(9): 1959 - 1969.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
I. Bady, C. Zitoun, L. Guignot, and G. Mithieux
Activation of liver G-6-Pase in response to insulin-induced hypoglycemia or epinephrine infusion in the rat
Am J Physiol Endocrinol Metab, April 1, 2002; 282(4): E905 - E910.
[Abstract] [Full Text] [PDF]


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