HIGHLIGHTED TOPIC Oxygen Sensing in Health and Disease Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors
HIGHLIGHTED TOPIC Oxygen Sensing in Health and Disease Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors
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发表时间：
2003
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通讯作者：
Dong-kyu Kim;N. Prabhakar;G. Kumar
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作者：
Dong-kyu Kim;N. Prabhakar;G. Kumar
Kim、Dong-Kyu、Nanduri R. Prabhakar 和 Ganesh K. Kumar。缺氧导致颈动脉体释放乙酰胆碱：自抑制受体参与的证据。 J Appl Physiol 96: 376–383, 2004。首次发表于 2003 年 8 月 15 日； 10.1152/ japplphyol.00726.2003.—本研究的目的是调查缺氧是否影响兔颈动脉体中乙酰胆碱（ACh）的释放，如果是的话，确定与这种反应相关的机制。电化学分析证明，ACh 在兔颈动脉体中表达（5.6±1.3 pmol/颈动脉体）。使用ACh特异性抗体对颈动脉体的原代培养物进行免疫细胞化学分析，进一步表明ACh样免疫反应性局限于许多血管球细胞。在从麻醉兔身上采集的离体颈动脉体中检查了缺氧对乙酰胆碱释放的影响。常氧（150 Torr）期间乙酰胆碱的基础释放量平均为 5.9 ± 0.5 fmol min 1 颈动脉体。将 PO2 降低至 90 和 20 Torr 分别逐渐减少 15% 和 68% 的乙酰胆碱释放。复氧后乙酰胆碱释放恢复至基础值。对多巴胺的同时监测显示，缺氧期间多巴胺的释放增加了六倍。高碳酸血症（21% O2 10% CO2）以及高钾（100 mM）促进颈动脉体释放乙酰胆碱，这表明缺氧引起的乙酰胆碱释放抑制并不是由于颈动脉体恶化所致。缺氧对培养基中的乙酰胆碱酯酶活性没有显着影响，这意味着乙酰胆碱酯酶水解的增加并不能解释缺氧诱导的乙酰胆碱酯酶释放抑制。在阿托品 (10 M) 或多潘立酮 (10 M) 存在下，缺氧刺激乙酰胆碱释放。这些结果表明，兔颈动脉体的血管球细胞表达ACh，并且缺氧通过激活颈动脉体中的毒蕈碱和多巴胺能自抑制受体来总体抑制ACh释放。
Kim, Dong-Kyu, Nanduri R. Prabhakar, and Ganesh K. Kumar. Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors. J Appl Physiol 96: 376–383, 2004. First published August 15, 2003; 10.1152/ japplphysiol.00726.2003.—The purpose of the present study was to investigate whether hypoxia influences acetylcholine (ACh) release from the rabbit carotid body and, if so, to determine the mechanism(s) associated with this response. ACh is expressed in the rabbit carotid body (5.6 1.3 pmol/carotid body) as evidenced by electrochemical analysis. Immunocytochemical analysis of the primary cultures of the carotid body with antibody specific to ACh further showed that ACh-like immunoreactivity is localized to many glomus cells. The effect of hypoxia on ACh release was examined in ex vivo carotid bodies harvested from anesthetized rabbits. The basal release of ACh during normoxia ( 150 Torr) averaged 5.9 0.5 fmol min 1 carotid body . Lowering the PO2 to 90 and 20 Torr progressively decreased ACh release by 15 and 68%, respectively. ACh release returned to the basal value on reoxygenation. Simultaneous monitoring of dopamine showed a sixfold increase in dopamine release during hypoxia. Hypercapnia (21% O2 10% CO2) as well as high K (100 mM) facilitated ACh release from the carotid body, suggesting that hypoxia-induced inhibition of ACh release is not due to deterioration of the carotid body. Hypoxia had no significant effect on acetylcholinesterase activity in the medium, implying that increased hydrolysis of ACh does not account for hypoxia-induced inhibition of ACh release. In the presence of either atropine (10 M) or domperidone (10 M), hypoxia stimulated ACh release. These results demonstrate that glomus cells of the rabbit carotid body express ACh and that hypoxia overall inhibits ACh release via activation of muscarinic and dopaminergic autoinhibitory receptors in the carotid body.