Nishi S, Seino Y, Takemura J, Ishida H, Seno M, Chiba T, Yanaihara C, Yanaihara N, Imura H
Am J Physiol. 1985 Apr;248(4 Pt 1):E425-31. doi: 10.1152/ajpendo.1985.248.4.E425.
The effect of electrical stimulation of the vagus nerves on the release of immunoreactive gastrin-releasing peptide (GRP), gastrin, and somatostatin was investigated using the isolated perfused rat stomach. Electrical stimulation (10 Hz, 1 ms duration, 10 V) of the peripheral end of the subdiaphragmatic vagal trunks produced a significant increase in both GRP and gastrin but a decrease in somatostatin. The infusion of atropine sulfate at a concentration of 10(-5) M augmented GRP release and reversed the decrease in somatostatin release in response to vagal stimulation to an increase above basal levels. However, the gastrin response to vagal stimulation was not affected by atropine. The infusion of hexamethonium bromide at a concentration of 10(-4) M significantly suppressed GRP release but did not affect gastrin secretion in response to vagal stimulation. On the other hand, the somatostatin response to vagal stimulation was completely abolished by hexamethonium. These findings lead us to conclude that the intramural GRP neurons might play an important role in the regulation of gastrin as well as somatostatin secretion and that somatostatin secretion may be controlled not only by a cholinergic inhibitory neuron but also by a noncholinergic, e.g., peptidergic stimulatory neuron, both of which may be regulated through preganglionic vagal fibers via nicotinic receptors. In addition, because the infusion of 10(-7) M GRP suppressed the somatostatin secretion, we suggest that either GRP should be excluded from the list of candidates for the noncholinergic stimulatory neurotransmitter for somatostatin secretion or that there are different mechanisms of action for endogenous and exogenous GRP.
利用离体灌注大鼠胃，研究了电刺激迷走神经对免疫反应性胃泌素释放肽（GRP）、胃泌素和生长抑素释放的影响。电刺激膈下迷走神经干外周端（10Hz，持续时间1ms，10V）可使GRP和胃泌素显著增加，但生长抑素减少。以10(-5)M的浓度输注硫酸阿托品可增强GRP释放，并使生长抑素释放因迷走神经刺激而产生的减少逆转，使其高于基础水平增加。然而，胃泌素对迷走神经刺激的反应不受阿托品影响。以10(-4)M的浓度输注溴化六甲铵可显著抑制GRP释放，但不影响迷走神经刺激引起的胃泌素分泌。另一方面，溴化六甲铵完全消除了生长抑素对迷走神经刺激的反应。这些发现使我们得出结论，壁内GRP神经元可能在胃泌素以及生长抑素分泌的调节中起重要作用，并且生长抑素分泌可能不仅受胆碱能抑制神经元控制，还受非胆碱能（例如肽能刺激神经元）控制，这两种神经元都可能通过节前迷走神经纤维经由烟碱受体进行调节。此外，由于输注10(-7)M GRP可抑制生长抑素分泌，我们建议要么将GRP从生长抑素分泌的非胆碱能刺激神经递质候选名单中排除，要么内源性和外源性GRP存在不同的作用机制。
