Effect of gastrin, histamine, serotonin, and adrenergic amines on gastroesophageal sphincter pressure in the dog

In nonrestrained dogs that had not been given chemicals and that were in the fasted and fed state, gastroesophageal sphincter pressure (GESP) was measured; results were compared with GESP induced in the same dogs by drugs that modified activity at cholinergic, adrenergic, histaminic, and gastrin receptors. Atropine reduced GESP from 38.5 +/- 1.3 (mean +/- SE) and 55.5 +/- 2.0 mm of Hg to 11.3 +/- 2.0 and 14.5 +/- 2.4 mm of Hg in fasted and fed dogs, respectively. Histamine induced phasic contractions that were not affected by anticholinergics or cimetidine. Iphenhydramine eliminated the phasic contractions and reduced GESP to 18.2 +/- 3.9 mm of Hg. In fed dogs, diphenhydramine reduced GESP to 37.0 +/- 2.5 mm of Hg, but cimetidine did not. Pentagastrin induced increases in GESP that were inversely related to basal GESP. Pentagastrin given during histamine infusion eliminated histamine-induced phasic contractions. In fed dogs, metoclopramide increased GESP from 48.8 +/- 4.0 mm of Hg to 76.0 +/- 4.0 mm of Hg; this increment was eliminated by diphenhydramine. Administration of atropine after metoclopramide reduced GESP the same as for dogs given atropine alone. An adrenergic amine with only alpha-adrenergic effects induced phasic contractions, and an adrenergic amine with only beta-adrenergic effects reduced GESP. Blockers of alpha and beta effects did not change GESP in fed dogs. Domperidone induced phasic contractions that were eliminated by feeding. Serotonin increased GESP. Canine GESP may be maintained in fed dogs by chemicals interacting with cholinergic, histaminic, gastrin, and serotonin receptors, but not by chemicals interacting with adrenergic receptors.