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Existence of NO-triggered vagal afferent activation in the rat gastric mucosa.

机译:大鼠胃黏膜中无触发的缩小传入活化的存在性。

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AIM: We previously reported the possible involvement of mucosal nitric oxide (NO)-triggered 5-HT release in luminal glutamate sensing by the gastric vagus nerve, and we proposed that the stomach, like the duodenum, could "taste" luminal nutrients. Nitric oxide synthase (NOS) is widely distributed in the gastric mucosa, but the physiological role of mucosal NO is not well understood. In this study, we investigated the functional coupling of NO and vagal nerve endings in the gastric mucosa. MAIN METHODS: For electrophysiological recordings, male Sprague-Dawley rats were anesthetized with urethane, and afferent nerve responses of rat vagal gastric branches to a NO donor were monitored. KEY FINDINGS: Intravenous application of 100microg/kg sodium nitroprusside (SNP) transiently increased afferent nerve discharges of the rat ventral gastric vagus, which was followed by rapid changes in blood pressure. High doses of SNP (>300microg/kg, i.v.) showed a biphasic increase in afferent discharges. Secondary activation of the vagal afferent continued even after blood pressure returned to basal levels. SNP-evoked afferent responses were abolished by mucosal 5-HT depletion using p-cholorophenylalanine and were inhibited by pre- and post-treatment with the 5-HT(3) antagonist granisetron. SIGNIFICANCE: These pharmacological results strongly indicate that NO-triggered 5-HT release is coupled to vagal afferent activation in the rat gastric mucosa.
机译:目的:我们之前报道了粘膜一氧化氮(NO)的可能参与 - 胃迷走神经中的腔谷氨酸感应中的5-HT释放,并提出胃,如十二指肠,可以“味道”腔营养素。一氧化氮合酶(NOS)广泛分布在胃粘膜中,但粘膜的生理作用不太清楚。在这项研究中,我们研究了胃粘膜中NO和迷住神经结束的功能偶联。主要方法:对于电生理记录,用氨基甲酸酯麻醉雄性Sprague-Dawley大鼠,并监测大鼠迷走胃分支对NO供体的传入神经反应。主要发现:静脉注射100microg / kg硝普钠(SNP)瞬时增加的大鼠腹侧胃腔的传入神经放电,随后是血压的快速变化。高剂量的SNP(> 300microg / kg,i.v.)显示出增殖放电的双相增加。即使血压恢复到基础水平后,缩小传入的二次活化也仍在继续。通过使用p-胆苯基丙氨酸的粘膜5-HT耗尽来消除了SNP诱发的传入反应,并通过用5-HT(3)拮抗剂格兰司琼预治疗和后处理抑制。意义:这些药理学结果强烈表示无触发的5-HT释放与大鼠胃粘膜中的缩小传入活化偶联。

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