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Effect of α 2 ‐adrenoceptor agonists on gastric pepsin and acid secretion in the rat
Author(s) -
TaziSaad Khaddouj,
Chariot Jacques,
Tacca Mario,
Rozé Claude
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb14414.x
Subject(s) - pepsin , guanabenz , secretion , endocrinology , medicine , gastric acid , chemistry , methacholine , receptor , biology , agonist , biochemistry , enzyme , respiratory disease , lung
1 The purpose of the present study was to analyze the effects of the α 2 ‐adrenoceptor agonists clonidine, guanabenz, detomidine and medetomidine on pepsin secretion in conscious rats provided with gastric chronic fistula and to compare this with acid secretion. 2 Basal interdigestive gastric secretion, which is mainly neurally driven in the rat, and the secretion directly stimulated by the two main stimulants of chief cells, cholecystokinin octapeptide (CCK8) and methacholine, were studied. 3 Basal secretion of pepsin and acid was inhibited by all four drugs with comparable EC 50 s. 4 CCK‐stimulated pepsin and acid secretion was less sensitive than basal pepsin and acid secretion to α 2 ‐adrenoceptor inhibition. 5 Methacholine‐stimulated pepsin and acid secretion was not changed by clonidine and guanabenz; methacholine‐stimulated acid was even marginally increased by clonidine. 6 These results do not favour the presence of α 2 ‐receptors on chief cells in the rat stomach. They rather suggest that pepsin inhibition by α 2 ‐adrenoceptor agonists is indirect and due to central or peripheral inhibition of the discharge of nerve fibres activating pepsin secretion.