Jpn. J. Pharmacol. 74 (1), 105-108 (1997)


Possible Mechanisms Underlying the Suppression of Gastric Vagal Afferents Due to Ecabapide (DQ-2511), a Gastroprokinetic Agent, in Rats

Satoshi Hatanaka (1), Akira Niijima (2) and Kazuhisa Furuhama (1)

(1) Tokyo Research and Development Center, Daiichi Pharmaceutical Co., Ltd.,16-13 Kitakasai 1-chome, Edogawa-ku,Tokyo 134, Japan
(2) Department of Physiology, Niigata University School of Medicine, Niigata 951, Japan

Abstract: We examined the implication of a nitric oxide (NO)-guanosine 3',5'-cyclic monophosphate (cGMP) cascade in the suppression of gastric vagal afferents due to ecabapide in anesthetized rats using a standard extracellular method of multi-unit recording. Sodium nitroprusside (SNP, 0.5 mg/kg), an NO donor, depressed the afferent discharge rate of the vagus nerve, like ecabapide (60 microg/kg). On the other hand, NG-nitro-L-arginine (L-NNA, 5 mg/kg), an NO biosynthesis inhibitor, significantly elevated its discharge rate. Pretreatment with L-NNA completely blocked the action of ecabapide. Atropine (0.05 mg/kg), a competitive antagonist of muscarinic cholinoceptors, showed no effect on the afferent firing. These results suggest that ecabapide may suppress the activation of vagal afferents in gastric inhibitory vago-vagal reflex pathways through the NO-cGMP cascade.

Keywords: Ecabapide (DQ-2511), Gastric vagal afferent, Nitric oxide-cGMP cascade


Copyrightę The Japanese Pharmacological Society 1997

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