Pathogenic Potential of Psychogenic Stress in Gastric Mucosal Injury

Abstract

Stress has been known to be a risk factor for gastric ulceration, but our understanding of the mechanisms constituting the pathogenic potential of stress is incomplete. In our experiments, psychogenic stress caused an inhibition of contractile activity (CA) in the antral and pyloric portion of the stomach and increase of CA in the duodenum. The stress-induced suppression of gastric CA persisted after blockade of muscarinic and nicotinic cholinoceptors, α2- and β1/β2-adrenoceptors. We suggested that the gastric CA suppression was resulted from the action of a hormonal stress factor (supposedly, corticotropin-releasing factor) on nonadrenergic inhibitory neurons of the enteric nervous system. The gastric motility inhibition could be, at least partly, resulted from the endocrine action of catecholamines circulating in blood on α-adrenoceptors of smooth muscle cells. Mechanisms of the stress-induced intensification of CA in the proximal and distal portion of the duodenum appeared to be different. The increase of CA in the proximal portion of the duodenum was preserved after blockade of muscarinic, nicotinic cholinceptors, and β1/β2-adrenoceptors. We suggested that the intensification of CA in the proximal duodenum was resulted from the direct action of a hormonal stress factor on smooth muscle cells. On the contrary, in the distal portion of the duodenum the blockade of muscarinic and nicotinic cholinceptors, and β1/β2-adrenoceptors abolished the stress-induced increase of CA. The intensification of CA of the distal portion of the duodenum was suggested to be mediated by the endocrine action of catecholamines on excitatory β-adrenoceptors located on the cholinergic neurons of the enteric nervous system. Increased CA of the duodenum under conditions of inhibited CA of the stomach may induce duodenogastric bile reflux, the latter being a pathogenic factor in the gastric mucosal injury. Thus, dysmotility in the gastroduodenal zone may be considered as a way for realization of the pathogenic potential of stress.