Vagal and splanchnic neural influences on gastric and duodenal bicarbonate secretions. An experimental study in the cat.
HCO3(-)-secretion by the gastroduodenal epithelium is probably an important factor in the mucosal defence against luminal H+. The aim of this study was to establish the existence of autonomic nervous influence on gastroduodenal HCO3(-)-secretion and to present some pharmacological characteristics. Experiments were performed on chloralosed cats with ligated adrenals. The vagal nerves were cut at the cervical level and arranged for electrical stimulation. The sympathetic splanchnic nerves were either cut or left intact. A gastric perfusion technique was developed which allowed simultaneous measurements of gastric motility and H+ and HCO3(-)-secretions, the latter being estimated from measurements of pH and pCO2 in the perfusate (isotonic NaCl). This technique was evaluated both ex vivo and in vivo. A distal segment of the duodenum was cannulated in situ and the lumen was perfused with recirculating isotonic NaCl. HCO3(-)-secretion into the perfusate was titrated by the pH-stat technique. Stimulation of the vagal nerves increased gastric and duodenal HCO3(-)-secretions and these responses were blocked completely by hexamethonium and partly inhibited by atropine. Vagally-induced increases in gastric and duodenal HCO3(-)-secretion were inhibited by: an intact splanchnic nerve supply, peripheral stimulation of the cut splanchnic nerves, and alpha-2-adrenoceptor stimulation with clonidine. In animals with intact splanchnic nerve supplies, the administration of the adrenolytic agent guanethidine or the alpha-2-adrenoceptor antagonist yohimbine revealed increases in gastric and duodenal HCO3(-)-secretion in response to vagal stimulation. Neither the alpha-1-adrenoceptor blocker prazosin nor the beta-adrenoceptor antagonist propranolol had any such effect. Furthermore, the inhibition of vagally induced gastric and duodenal HCO3(-)-secretion by splanchnic nerve stimulation or clonidine treatment was blocked by yohimbine. It can be concluded that peripheral autonomic nerves influence both gastric and duodenal HCO3(-)-secretion. The vagal nerves convey an excitatory pathway involving nicotinic, as well as muscarinic, cholinoceptor-mediated transmission. Furthermore, the present data suggest the existence of a sympatho-inhibitory mechanism for which the primary point of action involves alpha-2-adrenoceptors, presumably at a neural site.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D002415:Cats; D004386:Duodenum / Q000294:innervation*; D005260:Female; D005753:Gastric Mucosa / Q000294:innervation / Q000378:metabolism*; D005769:Gastrointestinal Motility / Q000187:drug effects; D007413:Intestinal Mucosa / Q000294:innervation / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D011950:Receptors, Cholinergic / Q000187:drug effects; D013153:Splanchnic Nerves / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D001639:Bicarbonates; D011950:Receptors, Cholinergic