Pharmacologic agents were used to study the role of the autonomic nervous system in the cytoprotection produced by intracisternal neurotensin against cold plus restraint stress-induced gastric ulcers in rats. Drugs which stimulated α- or β-adrenergic receptors or blocked muscarinic cholinergic receptors reduced the incidence of ulcers to a similar degree as intracisternal neurotensin; α-adrenergic or β-adrenergic blockade as well as cholinergic stimulation prevented neurotensin's beneficial effect. However, pretreatment with indomethacin blocked only the cytoprotective effect of neurotensin or β-adrenergic stimulation, but not that of muscarinic cholinergic blockade. In addition, pretreatment with reserpine or guanethidine also was effective in preventing cytoprotection by intracisternal neurotensin. These data indicate that the mechanism for cytoprotection by centrally administered neurotensin is mediated at least in part through activation of the sympathetic nervous system. This activation by neurotensin appears to produce cytoprotection by stimulation of gastric mucosal prostaglandin synthesis.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Psychiatry and Mental health
- Biological Psychiatry
- Endocrine and Autonomic Systems