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Titolo:
Regulatory mechanism of acid secretion in the damaged stomach: Role of endogenous nitric oxide
Autore:
Takeuchi, K; Araki, H; Kawauchi, S; Kunikata, T; Mizoguchi, H; Tashima, K;
Indirizzi:
Kyoto Pharmaceut Univ, Dept Pharmacol & Expt Therapeut, Kyoto 6078414, Japan Kyoto Pharmaceut Univ Kyoto Japan 6078414 herapeut, Kyoto 6078414, Japan
Titolo Testata:
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
, volume: 15, anno: 2000, supplemento:, S
pagine: D37 - D45
SICI:
0815-9319(200003)15:<D37:RMOASI>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
GASTRIC ALKALINE RESPONSE; RAT STOMACH; HISTAMINE-RELEASE; MAST-CELLS; SENSORY NEURONS; MILD IRRITANTS; MUCOSA; PROSTAGLANDINS; TAUROCHOLATE; RECEPTORS;
Keywords:
acid secretion; barrier disruption; calcium; histamine; nitric oxide; prostaglandin; stomach;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Takeuchi, K Kyoto Pharmaceut Univ, Dept Pharmacol & Expt Therapeut, Kyoto 6078414, Japan Kyoto Pharmaceut Univ Kyoto Japan 6078414 oto 6078414, Japan
Citazione:
K. Takeuchi et al., "Regulatory mechanism of acid secretion in the damaged stomach: Role of endogenous nitric oxide", J GASTR HEP, 15, 2000, pp. D37-D45

Abstract

The present article overviews the regulatory mechanism of acid secretion in the stomach after damage with taurocholate (TC), one of the bile acids. Mucosal exposure of a rat stomach to 20 mmol/L TC for 30 min caused a decrease of acid secretion with a concomitant increase in nitric oxide (NO) and prostaglandin (PG) E-2 (PGE(2)) as well as Ca2+ in the luminal contents. Prior administration of NG-nitro-L-arginine methyl ester (L-NAME), as well as indomethacin, significantly attenuated the reduction of acid secretion by TC and acid secretion was even increased in the presence of L-NAME. The acidstimulatory effect of L-NAME in the damaged stomach was not mimicked by aminoguanidine and was antagonized by co-administration of L-arginine but notD-arginine. Increased NO release in the damaged stomach was suppressed by pretreatment with L-NAME or co-application of EGTA and the latter also inhibited the increase in luminal Ca2+. The enhanced acid secretory response inthe presence of L-NAME was also inhibited by cimetidine, FPG-52694 (a mastcell stabilizer) or sensory deafferentation. Mucosal exposure to TC causedan increase in luminal histamine output, together with a decrease in the number of mucosal mast cells in the stomach. These changes were prevented byFPL-52694 and sensory deafferentation and were also partly suppressed by indomethacin. In addition, the acid stimulatory action of L-NAME in the damaged stomach was significantly mitigated when indomethacin was administered together with L-NAME. We conclude that: (i) damage in the stomach may activate acid a stimulatory pathway in addition to a PG-, NO- and Ca2+-dependentinhibitory mechanism, but the latter effect overcomes the former, resulting in a decrease in acid secretion; (ii) acid stimulation in the damaged stomach is mediated by histamine released from the mucosal mast cell, a process interacting with capsaicin-sensitive sensory nerves; (iii) the increase in luminal Ca2+ plays a role in increasing NO production and, hence, in regulating acid secretion; and (iv) PG may have a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect, probably through enhancing the release ofmucosal histamine. (C) 2000 Blackwell Science Asia Pty Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 00:47:41