Effects of nitric oxide inhibition on duodenal function in the rat:
involvement of neural mechanisms.
H[umlaut]allgren, Anneli, Gunnar Flemstr[diaeresis]om, Manaf Sababi,
and Olof Nylander.
Department of Physiology and Medical Biophysics, Biomedical Center,
Uppsala University, Uppsala, Sweden
APStracts 2:0059G, 1995.
This study examines the integrative response of several duodenal
functions to nitric oxide synthase inhibition. Effects of the nitric
oxide synthase inhibitor N-nitro-L-arginine-methyl-ester (L-NAME)
were studied in anesthetized rats, using in situ duodenal perfusion.
L-NAME increased bicarbonate secretion, permeability and fluid
secretion, and induced motility. Injection of L-arginine abolished L
-NAME-induced motility and lowered the secretion of bicarbonate and
fluid. Pretreatment with the nicotinic receptor antagonist
hexamethonium prevented the rise in bicarbonate secretion and
motility in response to L-NAME, but did not affect the increase in
mucosal permeability. Atropine diminished the L-NAME-induced
increases in permeability, motility and fluid secretion. The
adrenolytic drug guanethidine did not alter the responses to the
inhibitor. These results suggest that nitric oxide inhibits duodenal
motility and bicarbonate secretion by suppressing a stimulatory,
nicotinic receptor dependent, neural mechanism. The L-NAME-induced
contractions involve both a cholinergic, atropine-sensitive pathway
and non-adrenergic, non- cholinergic neural transmission. Muscarinic
receptors also mediate part of the L-NAME-induced increases in
mucosal permeability and fluid secretion.
Received 28 September 1994; accepted in final form 27 March 1995.
APS Manuscript Number G381-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 19 April 1995.