RT Journal Article
SR Electronic
T1 Inhibition of nitric oxide synthase delays gastric emptying of solid meals.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 660
OP 670
VO 271
IS 2
A1 M Orihata
A1 S K Sarna
YR 1994
UL http://jpet.aspetjournals.org/content/271/2/660.abstract
AB The role of nitric oxide (NO) was investigated in the regulation of gastric emptying of solid meals in six conscious dogs. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, significantly delayed gastric emptying. L-Arginine, the substrate of NO, given alone also significantly delayed gastric emptying compared with that in the saline control group but the delay with this chemical was significantly less than that with L-NAME. L-Arginine given with L-NAME significantly shortened the delay in gastric emptying caused by L-NAME. The delay in gastric emptying after the administration of L-NAME was primarily due to selective stimulation of the frequency of pyloric and proximal duodenal contractions without a concurrent change in antropyloroduodenal coordination. The delay in gastric emptying by L-arginine was primarily due to the suppression of gastric contractions. L-Arginine given with L-NAME completely reversed the motor effects of L-NAME. It was concluded that NO is a physiologic neurotransmitter of nonadrenergic, noncholinergic neurons in the stomach, pylorus and the duodenum that acts to regulate gastric emptying of solid meals. NO may facilitate gastric emptying by partially inhibiting pyloric and proximal duodenal contractions.