Abstract
Psychogenic stress in rabbits caused inhibition of contractile activity (CA) in antral and pyloric parts of the stomach. This reaction is preserved after blockade of a2-adrenergic receptors, β1/β2-adrenergic receptors, M or N-cholinergic receptors. We conclude that inhibition of gastric motility under stress is substantially «non-adrenergic non-cholinergic» and only in the initial phase of the reaction it appears to be «α-adrenergic». The latter mechanism also determines the initial transient inhibition of CA in duodenum. The subsequent strengthening of CA in the proximal duodenum is preserved after blockade of M or N-cholinergic receptors and is the result of direct exciting action of the endocrine stress factor on the smooth muscle of the gut. Strengthening of the CA in the distal duodenum is abolished by blockade of M or N-cholinergic receptors, as well as β1/β2-adrenergic receptors and is a consequence of the endocrine action of catecholamines on stimulating β-adrenergic receptors of enteric cholinergic neurons. The same mechanism is responsible for the initial increase of CA in jejunum, which is replaced by its inhibition, which is «non-adrenergic non-cholinergic». Inhibition of CA in the initial phase of the stress-induced response of the ileum, cecum and colon is due to «α-adrenergic» mechanism, and subsequent period of the CA inhibition is the result of the «non-adrenergic non-cholinergic» mechanism. Strengthening of the CA in the initial part of the distal colon is abolished by the blockade of M or N-cholinergic receptors, and is caused by the centrogenic stimulation of preganglionic neurons by endocrine stress factor with subsequent activation of effector cholinergic neurons of the enteric nervous system.
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