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Gastric relaxation and vasoactive intestinal peptide output in response to reflex vagal stimulation in the dog.
Author(s) -
Ito S,
Ohga A,
Ohta T
Publication year - 1988
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1988.sp017313
Subject(s) - hexamethonium , vasoactive intestinal peptide , reflex , vasodilation , vagus nerve , vagovagal reflex , stimulation , endocrinology , medicine , vagotomy , anesthesia , neuropeptide , receptor
1. Gastric relaxation, vasodilatation and vasoactive intestinal peptide (VIP) output from the stomach in response to stimulation of the central end of the cut vagus nerve were studied in anaesthetized dogs. 2. Central vagal stimulation (10 Hz, 40 V, 0.5 ms) normally produced a non‐adrenergic, non‐cholinergic (NANC) gastric relaxation via a vago‐vagal reflex. It also caused an increase followed by a decrease in gastric blood flow. 3. The increase in blood flow was attributable to a NANC gastric vasodilatation via a vago‐vagal reflex and the subsequent reduction in blood flow was decreased by splanchinicotomy. All these gastric and vascular responses were abolished by hexamethonium. 4. The gastric relaxation and vasodilatation induced by the vago‐vagal reflex had similar stimulation frequency‐response and pulse duration‐response relations. 5. Central vagal stimulation caused an increase in gastric venous VIP output which was abolished by vagotomy or hexamethonium but unaffected by splanchnicotomy. 6. VIP injected into the gastric artery mimicked the gastric relaxant and vasodilator responses to the vago‐vagal reflex. 7. We conclude that the intramural NANC inhibitory nerves activated by the vago‐vagal reflex release VIP which causes both gastric relaxation and vasodilatation.