Abstract
The effect of the nitric oxide (NO) synthase inhibitor, N G-nitro-L-arginine methyl ester (L-NAME) on the motility of the small intestine in an acute model in the anaesthetised rat was determined by changes in jejunal intraluminal pressure. L-NAME (0.5–10 mg kg −1 i.v.) caused a dose-dependent increase in intraluminal pressure and initiated phasic intestinal contractions. These responses were inhibited by concurrent administration of L-arginine (200 mg kg −1 i.v.) but not by D-arginine (200 mg kg −1). The increase in jejunal motility induced by L-NAME was attenuated by atropine (4 mg kg −1), although even high doses of atropine (16 mg kg −1) did not abolish these responses. This indicates that although there are interactions between NO and muscarinic cholinergic mechanisms, other processes are also involved in these contractile events following administration of L-NAME. These observations in the rat suggest that endogenous NO plays a role in the modulation of intestinal motility in vivo.
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