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Effect of Chronic Ethanol Ingestion on the Cyclic AMP System of the Upper Gastrointestinal Tract in the Rat
Author(s) -
Seitz H. K.,
Simon B.,
Czygan P.,
Veith S.,
Kommerell B.
Publication year - 1983
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1983.tb05485.x
Subject(s) - medicine , endocrinology , cyclase , adenylate kinase , phosphodiesterase , prostaglandin e2 , chemistry , ingestion , glucagon , adenosine , vasoactive intestinal peptide , ethanol , biology , hormone , neuropeptide , biochemistry , enzyme , stimulation , receptor
Chronic ethanol consumption significantly increases gastric adenyl‐ate cyclase (AC) activity ( p < 0.05) without influencing low K m 3′,5′‐cyclic adenosine monophosphate (cAMP) phosphodiesterase (PD) activity in the rat. On the other hand, in the duodenum and upper part of the jejunum, chronic ethanol feeding leads to a significant decrease of adenyiate cyclase activity ( p <0.02) and, again, does not affect low K m cAMP phosphodiesterase activity. In addition, the effect of various hormonal secretagoques on small intestinal adenylate cyclase activity was Investigated. Prostaglandin I 2 and D 2 , as well as glucagon, do not stimulate AC at all. However, small intestinal adenylate cyclase exhibits a lower sensitivity to prostaglandin E 2 and vasoactive intestinal peptide (VIP), and a lower efficacy to VIP after chronic ethanol consumption when compared to controls. The decrease of both basal and stimulated AC activity following ethanol ingestion in the upper small intestine may be due to membrane alterations and tissue damage caused by ethanol. The ethanol‐induced increase in gastric AC may be of relevance with respect to an increased acid secretion observed after alcohol administration.