Low glucose effects on rat carotid body chemoreceptor cells' secretory responses and action potential frequency in the carotid sinus nerve
Low glucose effects on rat carotid body chemoreceptor cells' secretory responses and action potential frequency in the carotid sinus nerve
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DOI：
10.1113/jphysiol.2007.144261
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发表时间：
2007-12-15
影响因子：
5.5
通讯作者：
Gonzalez, C.
中科院分区：
文献类型：
--
作者：
Conde, S. V.;Obeso, A.;Gonzalez, C.
葡萄糖剥夺（低血糖）通过神经内分泌反应来平衡，以诱导葡萄糖快速输送到血液中。一些中枢神经元可以感知葡萄糖，但最重要的葡萄糖传感器/血糖调节器位于大脑外部。最近在颈动脉体 (CB) 切片和培养中分离的化学感受器细胞中获得的一些实验证据支持 CB 在葡萄糖传感和可能的葡萄糖稳态中的作用，但由于低葡萄糖对颈动脉窦神经活动缺乏影响，这种作用受到质疑。这项工作的目的是澄清低血糖是否会刺激大鼠 CB 化学感受器。使用新鲜分离的完整 CB 制剂，我们监测了化学感受器细胞响应几种浓度的葡萄糖而释放的儿茶酚胺 (CA) 和 ATP，作为化学感受器细胞对血糖敏感性的指标，以及颈动脉窦神经 (CSN) 的电活动，作为 CB 反射触发输出的指标。我们观察到，在正常（5.55 mm）和低（3、1 和 0 mm）葡萄糖浓度存在的情况下，基础（20% O-2）和缺氧（7% 和 10% O-2）引起的 CA 释放是相同的。 0 mm 葡萄糖不会激活 CB 中 ATP 的释放，而缺氧 (5% O-2) 则可以。基础和缺氧 (5% O-2) 诱导的 CSN 动作电位频率与 5.55 和 1 mm 葡萄糖相同。我们的结果表明，低葡萄糖并不是对大鼠颈动脉体化学感受器的直接刺激。
Glucose deprivation (hypoglycaemia) is counterbalanced by a neuroendocrine response in order to induce fast delivery of glucose to blood. Some central neurons can sense glucose, but nevertheless the most important glucose sensors/glycaemia regulators are located outside the brain. Some recent experimental evidence obtained in carotid body (CB) slices and isolated chemoreceptor cells in culture supports a role for the CB in glucose sensing and presumably glucose homeostasis, but this role has been questioned on the basis of a lack of effect of low glucose on the carotid sinus nerve activity. This work was performed in an attempt to clarify if low glucose is or is not a stimulus for the rat CB chemoreceptors. Using freshly isolated intact CB preparations we have monitored the release of catecholamines (CAs) and ATP from chemoreceptor cells in response to several concentrations of glucose, as indices of chemoreceptor cell sensitivity to glycaemia, and the electrical activity in the carotid sinus nerve (CSN), as an index of reflex-triggering output of the CB. We have observed that basal (20% O-2) and hypoxia (7 and 10% O-2)-evoked release of CAs was identical in the presence of normal (5.55 mm) and low (3, 1 and 0 mm) glucose concentrations. 0 mm glucose did not activate the release of ATP from the CB, while hypoxia (5% O-2) did. Basal and hypoxia (5% O-2)-induced CSN action potential frequency was identical with 5.55 and 1 mm glucose. Our results indicate that low glucose is not a direct stimulus for the rat carotid body chemoreceptors.