Presynaptic sympathetic mechanism involved in the insulinostatic
effect of epinephrine in mouse pancreatic islets.
Karlsson, Sven, Ulrika Myrs[acute]en, Arie Nieuwenhuizen, Frank
Sundler, and Bo Ahr[acute]en.
Departments of Medicine, Malm[diaeresis]o and Physiology and
Neuroscience, Section of Neuroendocrine Cell Biology, Lund
University, Sweden
APStracts 3:0396R, 1996.
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 (VEHi) 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 (6
-OHDAi), indicating sympathetic denervation. Basal (5.6 mmol/l
glucose) or glucose-stimulated (16.7 mmol/l) insulin secretion did
not differ between incubated VEHi and 6-OHDAi. The insulinostatic
effect of epinephrine, but not that of norepinephrine, was markedly
impaired in 6-OHDAi (lowest effective insulinostatic concentration of
epinephrine was 0.01 nmol/l in VEHi and 1 nmol/l in 6-OHDAi). 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.
Received 31 July 1996; accepted in final form 15 October 1996.
APS Manuscript Number R445-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996