Lack of release of vasoactive intestinal polypeptide and calcitonin gene-related peptide during electrical stimulation of enteric nerves in streptozotocin-diabetic rats.

Hdl Handle:
http://hdl.handle.net/10142/92817
Title:
Lack of release of vasoactive intestinal polypeptide and calcitonin gene-related peptide during electrical stimulation of enteric nerves in streptozotocin-diabetic rats.
Authors:
Belai, A.; Lincoln, J.; Burnstock, G.
Abstract:
The simultaneous release of endogenous acetylcholine, serotonin, vasoactive intestinal polypeptide, substance P, and calcitonin gene-related peptide was measured during electrical field stimulation of isolated preparations of rat ileum from control and 8-wk streptozotocin-treated diabetic rats. Electrical field stimulation of the control rat ileum caused a significant increase in the release of all the above substances from the enteric nerves. The electrically evoked, but not the basal, release of these substances was inhibited by tetrodotoxin. In the diabetic rat ileum, however, there was no increase in the release of vasoactive intestinal polypeptide and calcitonin gene-related peptide during electrical stimulation, whereas endogenous release of acetylcholine, serotonin, and substance P was unaffected by the diabetic state. This was surprising in view of the increased fluorescence intensity and tissue content of vasoactive intestinal polypeptide-like immunoreactivity in the same tissue reported previously. The lack of increase in evoked release of vasoactive intestinal polypeptide in the diabetic preparations might be due to an impaired mechanism of release at the terminal site or to defective axonal transport of the peptide, whereas in the case of calcitonin gene-related peptide, it might be the result of the low level of the peptide present in the enteric nerve fibers of the diabetic rat ileum. The differential effect of diabetes on enteric nerves is discussed.
Citation:
Lack of release of vasoactive intestinal polypeptide and calcitonin gene-related peptide during electrical stimulation of enteric nerves in streptozotocin-diabetic rats. 1987, 93 (5):1034-40 Gastroenterology
Journal:
Gastroenterology
Issue Date:
Nov-1987
URI:
http://hdl.handle.net/10142/92817
PubMed ID:
2443415
Type:
Article
Language:
en
ISSN:
0016-5085
Appears in Collections:
Department of Life Sciences Collection

Full metadata record

DC FieldValue Language
dc.contributor.authorBelai, A.en
dc.contributor.authorLincoln, J.en
dc.contributor.authorBurnstock, G.en
dc.date.accessioned2010-02-23T23:06:52Z-
dc.date.available2010-02-23T23:06:52Z-
dc.date.issued1987-11-
dc.identifier.citationLack of release of vasoactive intestinal polypeptide and calcitonin gene-related peptide during electrical stimulation of enteric nerves in streptozotocin-diabetic rats. 1987, 93 (5):1034-40 Gastroenterologyen
dc.identifier.issn0016-5085-
dc.identifier.pmid2443415-
dc.identifier.urihttp://hdl.handle.net/10142/92817-
dc.description.abstractThe simultaneous release of endogenous acetylcholine, serotonin, vasoactive intestinal polypeptide, substance P, and calcitonin gene-related peptide was measured during electrical field stimulation of isolated preparations of rat ileum from control and 8-wk streptozotocin-treated diabetic rats. Electrical field stimulation of the control rat ileum caused a significant increase in the release of all the above substances from the enteric nerves. The electrically evoked, but not the basal, release of these substances was inhibited by tetrodotoxin. In the diabetic rat ileum, however, there was no increase in the release of vasoactive intestinal polypeptide and calcitonin gene-related peptide during electrical stimulation, whereas endogenous release of acetylcholine, serotonin, and substance P was unaffected by the diabetic state. This was surprising in view of the increased fluorescence intensity and tissue content of vasoactive intestinal polypeptide-like immunoreactivity in the same tissue reported previously. The lack of increase in evoked release of vasoactive intestinal polypeptide in the diabetic preparations might be due to an impaired mechanism of release at the terminal site or to defective axonal transport of the peptide, whereas in the case of calcitonin gene-related peptide, it might be the result of the low level of the peptide present in the enteric nerve fibers of the diabetic rat ileum. The differential effect of diabetes on enteric nerves is discussed.en
dc.language.isoenen
dc.subject.meshAcetylcholine-
dc.subject.meshAnimals-
dc.subject.meshCalcitonin-
dc.subject.meshCalcitonin Gene-Related Peptide-
dc.subject.meshDiabetes Mellitus, Experimental-
dc.subject.meshElectric Stimulation-
dc.subject.meshIleum-
dc.subject.meshMale-
dc.subject.meshNerve Fibers-
dc.subject.meshNeuropeptides-
dc.subject.meshRats-
dc.subject.meshRats, Inbred Strains-
dc.subject.meshSerotonin-
dc.subject.meshSplanchnic Nerves-
dc.subject.meshSubstance P-
dc.subject.meshVasoactive Intestinal Peptide-
dc.titleLack of release of vasoactive intestinal polypeptide and calcitonin gene-related peptide during electrical stimulation of enteric nerves in streptozotocin-diabetic rats.en
dc.typeArticleen
dc.identifier.journalGastroenterologyen
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