Abstract

Background. Until now, the effect of arginine vasopressin (AVP) in the DMV on gastric motility and the possible modulating pathway between the DMV and the gastrointestinal system remain poorly understood. Objectives. We aimed to explore the role of AVP in the DMV in regulating gastric motility and the possible central and peripheral pathways. Material and Methods. Firstly, we microinjected different doses of AVP into the DMV and investigated its effects on gastric motility in rats. Then, the possible central and peripheral pathways that regulate gastric motility were also discussed by microinjecting SR49059 (a specific AVP receptor antagonist) into the DMV and intravenous injection of hexamethonium (a specific neuronal nicotinic cholinergic receptor antagonist) before AVP microinjection. Results. Following microinjection of AVP (180 pmol and 18 pmol) into the DMV, the gastric motility (including total amplitude, total duration, and motility index of gastric contraction) was significantly inhibited (P < 0.05). Moreover, the inhibitory effect of AVP (180 pmol) on gastric motility could be blocked completely by both SR49059 (320 pmol) and hexamethonium (8 μmol). Conclusions. It is concluded that AVP inhibits the gastric motility by acting on the specific AVP receptor in the DMV, with the potential involvement of the parasympathetic preganglionic cholinergic fibers.

Highlights

  • Arginine vasopressin (AVP) is synthesized by the vasopressinergic neurons of paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus (SON) and plays important roles in water conservation, and so on

  • The inhibitory rates of AVP in group 1 microinjected into the dorsal motor nucleus of the vagus (DMV) for total duration, total amplitude, and motility index were 56.50%, 53.15%, and 56.08%, respectively

  • These percentages were higher than those of AVP in group 2, which suggested that the inhibitory effect of AVP on gastric motility showed a dose-dependent trend in the first 5 min after microinjection (Figures 3(d)–3(f))

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Summary

Introduction

Arginine vasopressin (AVP) is synthesized by the vasopressinergic neurons of paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus (SON) and plays important roles in water conservation, and so on. There were AVP and oxytocin (OT) receptors largely expressed in the soma and/or dendrite membranes of the activated neurons in the DMV [10, 11], suggesting the possible involvement of vasopressinergic/oxytocinergic projections from the PVN to the DMV in modulating the gastric functions. The effect of arginine vasopressin (AVP) in the DMV on gastric motility and the possible modulating pathway between the DMV and the gastrointestinal system remain poorly understood. We aimed to explore the role of AVP in the DMV in regulating gastric motility and the possible central and peripheral pathways. The possible central and peripheral pathways that regulate gastric motility were discussed by microinjecting SR49059 (a specific AVP receptor antagonist) into the DMV and intravenous injection of hexamethonium (a specific neuronal nicotinic cholinergic receptor antagonist) before AVP microinjection. It is concluded that AVP inhibits the gastric motility by acting on the specific AVP receptor in the DMV, with the potential involvement of the parasympathetic preganglionic cholinergic fibers

Objectives
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