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一氧化氮注入孤束核可阻断颈动脉化学感受器刺激引起的脑葡萄糖摄取。

Nitric oxide infused in the solitary tract nucleus blocks brain glucose retention induced by carotid chemoreceptor stimulation.

机构信息

Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico.

出版信息

Nitric Oxide. 2011 Nov 30;25(4):387-95. doi: 10.1016/j.niox.2011.09.003. Epub 2011 Sep 28.

DOI:10.1016/j.niox.2011.09.003
PMID:21983099
Abstract

Previous work has shown that the carotid body glomus cells can function as glucose sensors. The activation of these chemoreceptors, and of its afferent nucleus in the brainstem (solitary tract nucleus - STn), induces rapid changes in blood glucose levels and brain glucose retention. Nitric oxide (NO) in STn has been suggested to play a key role in the processing of baroreceptor signaling initiated in the carotid sinus. However, the relationship between changes in NO in STn and carotid body induced glycemic changes has not been studied. Here we investigated in anesthetized rats how changes in brain glucose retention, induced by the local stimulation of carotid body chemoreceptors with sodium cyanide (NaCN), were affected by modulation of NO levels in STn. We found that NO donor sodium nitroprusside (SNP) micro-injected into STn completely blocked the brain glucose retention reflex induced by NaCN chemoreceptor stimulation. In contrast, NOS inhibitor N(ω)-nitro-L-arginine methyl ester (L-NAME) increased brain glucose retention reflex compared to controls or to SNP rats. Interestingly, carotid body stimulation doubled the expression of nNOS in STn, but had no effect in iNOS. NO in STn could function to terminate brain glucose retention induced by carotid body stimulation. The work indicates that NO and STn play key roles in the regulation of brain glucose retention.

摘要

先前的工作表明,颈动脉体球细胞可以作为葡萄糖传感器发挥作用。这些化学感受器的激活及其在脑干中的传入核(孤束核 - STn)会导致血糖水平和脑葡萄糖摄取的快速变化。有人认为,STn 中的一氧化氮(NO)在颈动脉窦起始的压力感受器信号处理中发挥关键作用。然而,STn 中 NO 的变化与颈动脉体诱导的血糖变化之间的关系尚未得到研究。在这里,我们在麻醉大鼠中研究了局部刺激颈动脉体化学感受器(用氰化钠 - NaCN)引起的脑葡萄糖摄取变化如何受到 STn 中 NO 水平调节的影响。我们发现,将一氧化氮供体硝普酸钠(SNP)注入 STn 可完全阻断由 NaCN 化学感受器刺激引起的脑葡萄糖摄取反射。相比之下,NOS 抑制剂 N(ω)-硝基-L-精氨酸甲酯(L-NAME)与对照组或 SNP 大鼠相比,增加了脑葡萄糖摄取反射。有趣的是,颈动脉体刺激使 STn 中的 nNOS 表达增加了一倍,但对 iNOS 没有影响。STn 中的 NO 可能起到终止由颈动脉体刺激引起的脑葡萄糖摄取的作用。该工作表明,NO 和 STn 在调节脑葡萄糖摄取中发挥关键作用。

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引用本文的文献

1
Leptin in the Commissural Nucleus of the Tractus Solitarius (cNTS) and Anoxic Stimulus in the Carotid Body Chemoreceptors Increases cNTS Leptin Signaling Receptor and Brain Glucose Retention in Rats.孤束核中的瘦素(Leptin in the Commissural Nucleus of the Tractus Solitarius (cNTS))和颈动脉体化学感受器的缺氧刺激(Anoxic Stimulus in the Carotid Body Chemoreceptors)增加了孤束核瘦素信号受体(Leptin Signaling Receptor),并保留了大鼠大脑中的葡萄糖(Brain Glucose Retention in Rats)。
Medicina (Kaunas). 2022 Apr 16;58(4):550. doi: 10.3390/medicina58040550.