Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH.
Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH.
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人肾上腺肾小球细胞表达受 ANG II 和 ACTH 抑制的 K2P 和 GIRK 钾通道。
DOI：
10.1152/ajpcell.00118.2021
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Enyeart,JudithA
中科院分区：
文献类型：
--
作者：
Enyeart,JohnJ;Enyeart,JudithA
在全细胞膜片钳记录中，我们发现正常的人肾上腺肾小球带（AZG）细胞表达K+通道的三个主要家族成员。其中包括双孔（K2P）泄漏型和G蛋白偶联的内向整流（GIRK）通道，两者都受到刺激醛固酮分泌的肽激素的抑制。K2P电流显示的特性表明它是TREK-1 （KCNK2）。这种向外整流电流被花生四烯酸激活，并被血管紧张素II （ANG II）、促肾上腺皮质激素（ACTH）和福斯可林抑制。TREK-1的激活和抑制分别偶联于AZG细胞的超极化和去极化。第二个K2P通道TASK-1 （KCNK3）在AZG细胞中以较低的密度表达。人类AZG细胞也表达包括准瞬时和时间依赖性成分的内向整流K+电流（KIR）。这是首次从任何物种的AZG细胞中证实麒麟全细胞记录的存在。ANG II和ACTH选择性地抑制了时间依赖性电流，确定其为G蛋白偶联（GIRK）通道，最有可能是KIR3.4 （KCNJ5）。准瞬时kirk电流不受angii或ACTH的抑制，可能是一个单独的非girk电流。最后，AZG细胞表达电压门控的快速灭活K+电流，其特性被鉴定为KV1.4 (KCNA4)，这一结论被Northern blot证实。这些发现表明，人AZG细胞表达K2P和GIRK通道，ANG II和ACTH的抑制可能与去极化依赖性分泌有关。他们进一步证明，人类AZG K+通道与广泛采用的啮齿动物醛固酮分泌模型存在根本差异。
In whole cell patch clamp recordings, it was discovered that normal human adrenal zona glomerulosa (AZG) cells express members of the three major families of K+channels. Among these are a two-pore (K2P) leak-type and a G protein-coupled, inwardly rectifying (GIRK) channel, both inhibited by peptide hormones that stimulate aldosterone secretion. The K2P current displayed properties identifying it as TREK-1 (KCNK2). This outwardly rectifying current was activated by arachidonic acid and inhibited by angiotensin II (ANG II), adrenocorticotrophic hormone (ACTH), and forskolin. The activation and inhibition of TREK-1 was coupled to AZG cell hyperpolarization and depolarization, respectively. A second K2P channel, TASK-1 (KCNK3), was expressed at a lower density in AZG cells. Human AZG cells also express inwardly rectifying K+current(s) (KIR) that include quasi-instantaneous and time-dependent components. This is the first report demonstrating the presence of KIRin whole cell recordings from AZG cells of any species. The time-dependent current was selectively inhibited by ANG II, and ACTH, identifying it as a G protein-coupled (GIRK) channel, most likely KIR3.4 (KCNJ5). The quasi-instantaneous KIRcurrent was not inhibited by ANG II or ACTH and may be a separate non-GIRK current. Finally, AZG cells express a voltage-gated, rapidly inactivating K+current whose properties identified as KV1.4 (KCNA4), a conclusion confirmed by Northern blot. These findings demonstrate that human AZG cells express K2P and GIRK channels whose inhibition by ANG II and ACTH is likely coupled to depolarization-dependent secretion. They further demonstrate that human AZG K+channels differ fundamentally from the widely adopted rodent models for human aldosterone secretion.
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