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1 Neuroscience, Pennington Biomedical Research Center-LSU System, Baton Rouge, Louisiana, USA
* To whom correspondence should be addressed. E-mail: HermanGE{at}pbrc.edu.
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 (TH-IR) cells, while the DMV response involves both an
1 excitatory and an
2 inhibitory response. In the present study, with the use of an esophageal balloon distention to evoke gastric relaxation (esophageal-gastric reflex = EGR), we investigated the peripheral pharmacologic 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, while 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 amplitude of induced EGR is quite comparable (4.3 ± 2.6%) to that seen when the animal is pretreated with the nicotinic ganglionic blocker, hexamethonium. In the presence of bethanechol, the amplitude of the esophageal-distention induced gastric relaxation was increased to 177.0 ± 10.0% of control; administration of L-NAME reduced the amplitude of the gastric relaxation 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.
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