Golovinska Y. The role of peripheral glutamate receptors of NMDA-subtype in regulation of gastric acid secretion in rats

Object: gastric acid secretion (GAS). Objective: to study the effect of the activation and localization of NMDA-receptors on basal and stimulated GAS in rat stomach. Methods: investigations were carried out in 429 white rats in conditions of acute experiment. GAS was determined in urethane-anesthetized animals using gastric perfusion method described by Ghosh and Shild. It was studied the effects of N-methyl-D-aspartate on basal and stimulated GAS. GAS was stimulated by histamine, pentagastrin, carbachol, cytisine, insulin and by 2-deoxy-D-glucose. Blockers used: pentamine, atropine, gastrotsepin, proglumide and ranitidine. Perform surgical vagotomy. Gastric acidity was determined by automatic titration method of 0,01 N sodium hydroxide solution. Results: results obtained in the study of peripheral glutamate NMDA-subtype receptors broaden the understanding of the functioning of the peripheral nervous system. Establishing the role of NMDA-receptors in the regulation of gastric secretion of acid may be a promising basis for the production of more effective drugs that have no adverse effect on gastric secretion. The results of the disertation work are included in the education process at the Department of Physiology of Man and Animals of ECC "Biology Institute" Taras Shevchenko Kyiv National University. Novelty: the first was found in the work that peripheral glutamate NMDA-subtype receptors does not participate in the regulation of the stimulated by histamine, pentagastrin, cytisine, insulin and 2-deoxy-D-glucose GAS. Peripheral NMDA-receptors are involved in the regulation of carbachol GAS, vagotomy does not influence this effect. Pentamin, atropine, gastrotsepin, proglumid and ranitidine eliminated the amplifying effect of N-methyl-D-aspartate on carbachol GAS. The data obtained allowed to conclude that the excitation of NMDA-receptor is required membrane depolarization cholinergic, which localized this receptor. Acetylcholine or carbachol that affect the M1-acetylcholine receptors cause this depolarization. Scope of use: physiology, pharmacology, biophysics.