Aim: 

to compare the influence of channel blocker MK-801 and the blocker of polyamine site arcaine of NMDA-receptors on stimulated gastric acid secretion (GAS).

Methods: 

The investigations were carried out on white male rats in acute experiments by method of perfusion of isolated stomach by Ghosh and Shild. The GAS was stimulated by intraperitoneal (i.p.) injection of carbacholin (0.01 mg/ kg) and pentagastrin (0.026 mg/ kg). MK-801 was injected in dose 0.1 mg/ kg, i.p., arcaine – in dose 10 mg/ kg, i.p. One experimental group of animals was vagotomised and treated with MK-801.

Results: 

It was established that blockade of polyamine site of NMDA-receptors by arcaine suppressed carbacholin GAS by 79% (P < 0.001) and pentagastrin GAS by 36% (P < 0.001). MK-801 diminished carbacholin GAS by 37% (P < 0.01) and did not influence pentagastrin GAS. Increasing effect of MK-801 on carbacholin GAS is abolished by vagotomy. So, in realisation GAS are involved central glutamate receptors that are localised on the neurons of nucleus tractus solitarii (NTS). Parietal cells have own receptors for gastrin, but realisation of GAS, stimulated by pentagastrin are controlled by strong cholinergic stimulus of the vagus. We suggest that excitation of polyamine site of central NMDA-receptors by endogenous glutamate by vagus passes to intrinsic mucosa and increases GAS, stimulated by pentagastrin.

Conclusion: 

Excitation of ion channel and polyamine site NMDA-receptors by endogenous glutamate are important for realization of GAS stimulated by carbacholin. But for realisation of pentagastrin GAS is necessary stimulation only polyamine site by endogenous glutamate.