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Am J Physiol Regul Integr Comp Physiol 290: R1570-R1576, 2006. First published January 26, 2006; doi:10.1152/ajpregu.00717.2005
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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Esophageal-gastric relaxation reflex in rat: dual control of peripheral nitrergic and cholinergic transmission

Gerlinda E. Hermann, R. Alberto Travagli, and Richard C. Rogers

Department of Neuroscience, Pennington Biomedical Research Center-Louisiana State University System, Baton Rouge, Louisiana

Submitted 7 October 2005 ; accepted in final form 17 January 2006

It has long been known that the esophageal distension produced by swallowing elicits a powerful proximal gastric relaxation. Gastroinhibitory control by the esophagus involves neural pathways from esophageal distension-sensitive neurons in the nucleus tractus solitarius centralis (cNTS) with connections to virtually all levels of the dorsal motor nucleus of the vagus (DMV). We have shown recently that cNTS responses are excitatory and primarily involve tyrosine hydroxylase-immunoreactive cells, whereas the DMV response involves both an {alpha}1 excitatory and an {alpha}2 inhibitory response. In the present study, using an esophageal balloon distension to evoke gastric relaxation (esophageal-gastric reflex, EGR), we investigated the peripheral pharmacological basis responsible for this reflex. Systemic administration of atropine methyl nitrate reduced the amplitude of the gastric relaxation to 52.0 ± 4.4% of the original EGR, whereas NG-nitro-L-arginine methyl ester (L-NAME) reduced it to 26.3 ± 7.2% of the original EGR. Concomitant administration of atropine methyl nitrate and L-NAME reduced the amplitude of the gastric relaxation to 4.0 ± 2.5% of control. This reduction in the amplitude of induced EGR is quite comparable (4.3 ± 2.6%) to that seen when the animal was pretreated with the nicotinic ganglionic blocker hexamethonium. In the presence of bethanechol, the amplitude of the esophageal distension-induced gastric relaxation was increased to 177.0 ± 10.0% of control; administration of L-NAME reduced this amplitude to 19.9 ± 9.5%. Our data provide a clear demonstration that the gastroinhibitory control by the esophagus is mediated via a dual vagal innervation consisting of inhibitory nitrergic and excitatory cholinergic transmission.

receptive relaxation reflex; nonadrenergic, noncholinergic; vagovagal reflex


Address for reprint requests and other correspondence: G. E. Hermann, Pennington Biomedical Research Center, 6400 Perkins Rd., Baton Rouge, LA 70808 (e-mail: hermange{at}pbrc.edu)




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