Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells.
Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells.
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大鼠颈动脉体肾小球细胞中非选择性阳离子通道的电压和受体介导的激活。
DOI：
10.1016/j.resp.2016.12.005
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发表时间：
2017-03
影响因子：
2.3
通讯作者：
Kim D
中科院分区：
文献类型：
--
作者：
Wang J;Hogan JO;Kim D
最近的研究表明，缺氧激活颈动脉血管球细胞中Ca2+敏感，Na+渗透性非选择性阳离子通道（NSC）。我们研究了通过Ca2+通道（Cav）增加Ca2+内流的线粒体抑制剂和从内质网（ER）释放Ca2+的受体激动剂对NSC的影响。线粒体抑制剂（NaCN， FCCP, H2S， NO）升高[Ca2+]i并激活NSC。血管紧张素II和乙酰胆碱通过Gq-IP3途径升高[Ca2+]i激活NSC。然而，内皮素-1 （Gq）和5-HT （Gq）对[Ca2+]i的影响很小或没有影响，也没有激活NSC。腺苷（Gs）引起[Ca2+]i的微弱升高，但不激活NSC。多巴胺（Gs）和γ-氨基酪酸（Gi）对[Ca2+]i升高无效，不能激活NSC。储存操作的Ca2+进入（SOCE）是由环吡唑酸激活的NSC消耗Ca2+储存而产生的。我们的研究结果表明，Ca2+通过Cav进入，ER Ca2+释放和SOCE可以激活NSC。因此，NSC有助于电压和受体介导的血管球细胞兴奋。
Recent study showed that hypoxia activates a Ca2+-sensitive, Na+-permeable non-selective cation channel (NSC) in carotid body glomus cells. We studied the effects of mitochondrial inhibitors that increase Ca2+ influx via Ca2+ channel (Cav), and receptor agonists that release Ca2+ from endoplasmic reticulum (ER) on NSC. Mitochondrial inhibitors (NaCN, FCCP, H2S, NO) elevated [Ca2+]i and activated NSC. Angiotensin II and acetylcholine that elevate [Ca2+]i via the Gq-IP3 pathway activated NSC. However, endothelin-1 (Gq) and 5-HT (Gq) showed little or no effect on [Ca2+]i and did not activate NSC. Adenosine (Gs) caused a weak rise in [Ca2+]i but did not activate NSC. Dopamine (Gs) and γ-aminobytyric acid (Gi) were ineffective in raising [Ca2+]i and failed to activate NSC. Store-operated Ca2+ entry (SOCE) produced by depletion of Ca2+ stores with cyclopiazonic acid activated NSC. Our results show that Ca2+ entry via Cav, ER Ca2+ release and SOCE can activate NSC. Thus, NSC contributes to both voltage- and receptor-mediated excitation of glomus cells.