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单个球细胞中离子通道的氧感应与化学转导

Oxygen sensing by ion channels and chemotransduction in single glomus cells.

作者信息

Montoro R J, Ureña J, Fernández-Chacón R, Alvarez de Toledo G, López-Barneo J

机构信息

Departamento de Fisiología Médica y Biofísica, Universidad de Sevill

出版信息

J Gen Physiol. 1996 Jan;107(1):133-143. doi: 10.1085/jgp.107.1.133.

DOI:10.1085/jgp.107.1.133
PMID:8741735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2219248/
Abstract

We have monitored cytosolic [Ca2+] and dopamine release in intact fura-2-loaded glomus cells with microfluoroimetry and a polarized carbon fiber electrode. Exposure to low PO2 produced a rise of cytosolic [Ca2+] with two distinguishable phases: an initial period (with PO2 values between 150 and approximately 70 mm Hg) during which the increase of [Ca2+] is very small and never exceeds 150-200 nM, and a second phase (with PO2 below approximately 70 mm Hg) characterized by a sharp rise of cytosolic [Ca2+]. Secretion occurs once cytosolic [Ca2+] reaches a threshold value of 180 +/- 43 nM. The results demonstrate a characteristic relationship between PO2 and transmitter secretion at the cellular level that is comparable with the relation described for the input (O2 tension)output (afferent neural discharges) variables in the carotid body. Thus, the properties of single glomus cells can explain the sensory functions of the entire organ. In whole-cell, patch-clamped cells, we have found that in addition to O2-sensitive K+ channels, there are Ca2+ channels whose activity is also regulated by PO2. Ca2+ channel activity is inhibited by hpoxia, although in a strongly voltage-dependent manner. The average hypoxic inhibition of the calcium current in 30% +/- 10% at -20 mV but only 2% +/- 2% at +30 mV. The differential inhibition of K+ and Ca2+ channels by hypoxia helps to explain why the secretory response of the cells is displaced toward PO2 values (below approximately 70 mm Hg) within the range of those normally existing in arterial blood. These data provide a conceptual framework for understanding the cellular mechanisms of O2 chemotransduction in the carotid body.

摘要

我们使用显微荧光测定法和极化碳纤维电极,监测了完整的、负载fura - 2的球细胞中的胞质[Ca2+]和多巴胺释放。暴露于低氧分压会使胞质[Ca2+]升高,呈现出两个可区分的阶段:初始阶段(氧分压值在150至约70毫米汞柱之间),在此期间[Ca2+]的增加非常小,且从未超过150 - 200纳摩尔;第二阶段(氧分压低于约70毫米汞柱),其特征是胞质[Ca2+]急剧上升。当胞质[Ca2+]达到180±43纳摩尔的阈值时,分泌就会发生。结果表明,在细胞水平上,氧分压与递质分泌之间存在一种特征关系,这与颈动脉体中描述的输入(氧张力)-输出(传入神经放电)变量之间的关系相当。因此,单个球细胞的特性可以解释整个器官的感觉功能。在全细胞膜片钳记录的细胞中,我们发现除了对氧敏感的钾通道外,还有钙通道,其活性也受氧分压调节。缺氧会抑制钙通道活性,尽管这种抑制具有强烈的电压依赖性。在 - 20毫伏时,钙电流的平均缺氧抑制率为30%±10%,但在 + 30毫伏时仅为2%±2%。缺氧对钾通道和钙通道的差异性抑制有助于解释为什么细胞的分泌反应会朝着动脉血中正常存在的氧分压值范围(低于约70毫米汞柱)偏移。这些数据为理解颈动脉体中氧化学转导的细胞机制提供了一个概念框架。

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