Potentiation of gastrin and histamine stimulated acid secretion in Heidenhain pouches by distention--an atropine-resistant mechanism.
1. Distention of the vagally denervated fundic gland area, although by itself a generally ineffective stimulus to acid secretion in this study, will markedly increase the acid secretory response to stimulation by endogenous gastrin, pentagastrin and histamine. Even maximal responses to histamine can be increased, thus demonstrating true potentiation between distention and humoral stimuli. 2. The magnitude of the distention potentiation does not appear to be influenced by the nature of the background stimulus or the background level of secretion. 3. The distention potentiation of the response to histamine is reduced but not abolished by intravenous atropine and hexamethonium. Thus, there appear to be two components to the local distention mechanism. One is cholinergic, the other, atropine-resistant component is possibly non-cholinergic. At least one of these components, possibly the cholinergic, involves a nicotinic synapse in its pathway.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D003714:Denervation; D004285:Dogs; D004357:Drug Synergism; D005260:Female; D013271:Gastric Dilatation / Q000378:metabolism; D005750:Gastric Juice / Q000378:metabolism*; D005755:Gastrins / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D008297:Male; D010418:Pentagastrin / Q000494:pharmacology; D013270:Stomach / Q000294:innervation / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology
D005755:Gastrins; D001285:Atropine; D006632:Histamine; D010418:Pentagastrin