Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats.

Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats.
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乙酰胆碱增加成年猫动脉化学感受器细胞的细胞内钙。

DOI:
10.1152/jn.1997.78.5.2388
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发表时间:
1997
期刊:
Journal of neurophysiology.
影响因子:
--
通讯作者:
Sham,JS
Sham,JS
中科院分区:
--
文献类型:
--
作者:
Shirahata,M;Fitzgerald,RS;Sham,JS

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放大图片作者:Robert S. Fitzgerald和James S. K.假的。乙酰胆碱增加成年猫动脉化学感受器细胞的细胞内钙。神经生理学杂志。78:2388-2395,1997。一些神经递质已被报道在颈动脉体的化学感受中发挥重要作用。其中,乙酰胆碱(ACh)似乎参与猫颈动脉体的兴奋过程。作为阐明ACh在猫颈动脉体化学感受中的可能作用的步骤之一,我们研究了ACh对培养的颈动脉体细胞内钙浓度([Ca 2 +]i)的影响。分离成年猫颈动脉体,培养2周。[Ca2+] i用Indo-1 AM用显微荧光技术从细胞簇中测量。实验在37°C下进行,并且细胞用用5%C02 - 16%02 - 79%N2平衡的改良Krebs溶液连续灌流。ACh(100 μM)引起约70%的细胞团[Ca ~(2+)] i显著升高,1-300 μM的ACh对[Ca ~(2+)] i的反应呈浓度依赖性。乙酰胆碱反应的幅度和动力学模拟尼古丁的应用,而毒蕈碱激动剂,毛果芸香碱,和毒蕈碱未能引起类似的反应。ACh诱导的[Ca ~(2+)] i增加依赖于细胞外Ca ~(2+):瞬时去除细胞外Ca ~(2+)可使[Ca ~(2+)] i显著降低或完全消除。咖啡因(5 mM)或硝苯地平(10 μM)可持续但仅部分降低反应。美加明(100 μM)的作用是抑制性的,但很小。此外,增加[Ca 2 +] i响应ACh也观察到在一些集群,不响应高K(100 mM)Krebs。上述结果提示,ACh通过激活神经元烟碱型ACh受体,使细胞内Ca ~(2+)内流增加。此外,其他途径,如Ca ~(2+)通过L-型钙通道内流,可能继发于膜去极化,和Ca ~(2+)从细胞内库释放可能参与ACh引起的[Ca ~(2+)] i增加。毒蕈碱受体似乎只起很小的作用,如果有的话。
Shirahata, Machiko, Robert S. Fitzgerald, and James S. K. Sham.Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats.J. Neurophysiol.78: 2388–2395, 1997. Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca2+]i) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca2+]iwas measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37°C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O2-79% N2. ACh (100 μM) caused a marked increase in [Ca2+]iin ∼70% of clusters, and the responses to 1–300 μM of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca2+]iwas dependent on extracellular Ca2+: it was greatly reduced or completely abolished by a transient removal of extracellular Ca2+. The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 μM). The effect of mecamylamine (100 μM) was inhibitory but small. Moreover, the increase in [Ca2+]iin response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca2+]iof cultured carotid body cells by activating neuronal nicotinic ACh receptors, leading to Ca2+influx via nicotinic channels. In addition, other pathways such as Ca2+influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca2+release from intracellular stores may participate in increasing [Ca2+]iin response to ACh. Muscarinic receptors appear to play only a small role, if any.
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