Involvement of endogenous nitric oxide in the inhibition by endotoxin and interleukin-1 beta of gastric acid secretion

Esplugues, J.V.; Martínez-Cuesta, M.A.; Barrachina, M.D.; Calatayud, S.; Whittle, B.J.

Journal of Gastroenterology and Hepatology 9(Suppl 1): S45-S49

1994


ISSN/ISBN: 0815-9319
PMID: 7881019
DOI: 10.1111/j.1440-1746.1994.tb01301.x
Accession: 043465872

Download citation:  
Text
  |  
BibTeX
  |  
RIS

Article/Abstract emailed within 0-6 h
Payments are secure & encrypted
Powered by Stripe
Powered by PayPal

Abstract
Administration of Escherichia coli endotoxin abolished the acid secretory response induced by a bolus injection of pentagastrin in the continuously perfused stomach of the anaesthetized rat. Likewise, acid secretion stimulated by the continuous intravenous perfusion of pentagastrin was inhibited by administration of interleukin-1 beta (IL-1 beta). In both cases pretreatment with NG-nitro-L-arginine methyl ester (L-NAME) but not dexamethasone or indomethacin substantially restored the secretory responses to pentagastrin. The actions of L-NAME were reversed by the prior administration of L-arginine but not by its enantiomer D-arginine. Even though L-NAME increased blood pressure, this does not seem to be the mechanism by which endotoxin-induced acid inhibition was prevented, since similar systemic pressor responses induced by phenylephrine had no such effect. The secretory response elicited by pentagastrin in the isolated lumen perfused stomach of the rat was not influenced by incubation (100 min) with IL-1 beta. These observations suggest that the acute inhibition of acid responses to pentagastrin by endotoxin and IL-1 beta involves nitric oxide (NO) synthesis from L-arginine.

Involvement of endogenous nitric oxide in the inhibition by endotoxin and interleukin-1 beta of gastric acid secretion