Effects of pharmacological lesion of adrenergic innervation of the dorsal vagal nucleus on pancreatic insulin secretion in normal and vagotomized rats
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
8789641
Knihovny.cz E-resources
- MeSH
- Glucose pharmacology MeSH
- Insulin blood metabolism MeSH
- Blood Glucose analysis MeSH
- Rats MeSH
- Islets of Langerhans metabolism MeSH
- Medulla Oblongata physiology MeSH
- Vagus Nerve physiology MeSH
- Oxidopamine pharmacology MeSH
- Rats, Sprague-Dawley MeSH
- Insulin Secretion MeSH
- Sympathectomy, Chemical MeSH
- Sympatholytics pharmacology MeSH
- Vagotomy MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Glucose MeSH
- Insulin MeSH
- Blood Glucose MeSH
- Oxidopamine MeSH
- Sympatholytics MeSH
Previous morphological and physiological studies have suggested that the adrenergic innervation of the dorsal motor nucleus of the vagus nerve (dmnX) is involved in direct synaptic inhibition of parasympathetic preganglionic neurones of the vagus that control secretion of pancreatic insulin. We investigated the effects of bilateral 6-hydroxydopamine (6-OHDA) lesions of adrenergic innervation of the dmnX on pancreatic insulin secretion and glycaemia in normal and vagotomized rats. After two weeks the 6-OHDA lesions produced a marked increase in circulating insulin levels, but no change in glycaemia. Hyperinsulinaemia after adrenergic denervation of the dmnX was more pronounced when a glucose bolus was injected intraarterially. Bilateral subdiaphragmatic vagotomy reversed the observed hyperinsulinaemia. This targeted pharmacological lesion of the adrenergic innervation of dmnX thus causes hypersecretion by pancreatic B cells, an effect which requires an intact vagus nerve.