Nervous control of the release of neurotensin-like immunoreactivity from the small intestine of the rat.
Intraduodenal administration of oleic acid increased plasma neurotensin-like immunoreactivity (p-NTLI). The integrated responses to saline and oleic acid were 5.7 and 9.7 nM0-180 min, respectively. The integrated response was not significantly altered by i.v. administration of atropine, guanethidine, mepyramine, cimetidine, methysergide or a substance P antagonist, but it was abolished by hexamethonium and morphine (5.9 and 6.3 nM0-180 min, respectively). An exogenous supply of bile and pancreatic juice did not alter the integrated response in morphine- and hexamethonium-treated rats. Haloperidol significantly increased the p-NTLI response to oleic acid (13 nM0-180 min). The results suggest that the release of neurotensin is influenced by nervous pathways involving nicotinic and opioid receptors. Catecholamines and 5-HT receptors may exert an inhibitory influence on the release of NTLI.
D000818:Animals; D007421:Intestine, Small / Q000294:innervation / Q000378:metabolism*; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D009479:Neuropeptides; D009829:Oleic Acids / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011978:Receptors, Nicotinic / Q000187:drug effects*; D011957:Receptors, Opioid / Q000187:drug effects*; D012965:Sodium Chloride / Q000494:pharmacology
D009419:Nerve Tissue Proteins; D009479:Neuropeptides; D009829:Oleic Acids; D011978:Receptors, Nicotinic; D011957:Receptors, Opioid; C031644:neurotensin-like immunoreactivity; D012965:Sodium Chloride