Studies on the mechanisms by which (Gln4)-neurotensin reduces lower esophageal sphincter (LES) pressure in man.
The mechanisms behind the reduction of lower esophageal sphincter (LES) pressure by (Gln4)-neurotensin were investigated in 17 healthy volunteers. LES pressure was measured with a continuous pull-through technique. Intravenous infusion of (Gln4)-neurotensin (6, 12 or 18 pmol X kg-1 X min-1) caused a significant, prompt and dose-related fall in LES pressure from a mean basal value of 35.2 +/- 3.4 mmHg to 29.2 +/- 3.0, 27.3 +/- 3.5 and 25.9 +/- 2.7 mmHg, respectively. Atropine (1 mg) administered as a single i.v. bolus injection did not change the mean pressure significantly. After atropine, the LES pressure response to 12 pmol X kg-1 X min-1 of (Gln4)-neurotensin was abolished. The increase in LES pressure following a bolus injection of pentagastrin (0.6 microgram X kg-1) was not inhibited by 12 pmol X kg-1 X min-1 of (Gln4)-neurotensin. The concentration of plasma neurotensin-like immunoreactivity (p-NTLI) in all experiments was lower than, or in the same order of magnitude as, that obtained postprandially. Thus, the data indicate that reduction of LES pressure by neurotensin may occur postprandially and that this effect seems to involve a cholinergic nervous pathway, rather than being due to a direct myogenic action.
D000328:Adult; D001285:Atropine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004943:Esophagogastric Junction / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D008297:Male; D009496:Neurotensin / Q000031:analogs & derivatives* / Q000494:pharmacology; D010418:Pentagastrin / Q000494:pharmacology; D011312:Pressure
D009496:Neurotensin; C028737:neurotensin, Gln(4)-; D001285:Atropine; D010418:Pentagastrin