| http://purl.uniprot.org/citations/34038243 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/34038243 | http://www.w3.org/2000/01/rdf-schema#comment | "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 KIR in 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 KIR current 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."xsd:string |
| http://purl.uniprot.org/citations/34038243 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpcell.00118.2021"xsd:string |
| http://purl.uniprot.org/citations/34038243 | http://purl.uniprot.org/core/author | "Enyeart J.J."xsd:string |
| http://purl.uniprot.org/citations/34038243 | http://purl.uniprot.org/core/author | "Enyeart J.A."xsd:string |
| http://purl.uniprot.org/citations/34038243 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
| http://purl.uniprot.org/citations/34038243 | http://purl.uniprot.org/core/name | "Am J Physiol Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/34038243 | http://purl.uniprot.org/core/pages | "C158-C175"xsd:string |
| http://purl.uniprot.org/citations/34038243 | http://purl.uniprot.org/core/title | "Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH."xsd:string |
| http://purl.uniprot.org/citations/34038243 | http://purl.uniprot.org/core/volume | "321"xsd:string |
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