The antimalarial agent mefloquine inhibits ATP-sensitive K-channels
The antimalarial agent mefloquine inhibits ATP-sensitive K-channels
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DOI:
10.1038/sj.bjp.0703638
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发表时间:
2000-10-01
影响因子:
7.3
通讯作者:
Ashcroft, FM
中科院分区:
文献类型:
--
作者:
Gribble, FM;Davis, TME;Ashcroft, FM
1 The aim of this study was to determine whether antimalarial agents inhibit ATP-sensitive potassium (K-ATP) channels and thereby contribute to the observed side-effects of these drugs.2 Mefloquine (10-100 muM), but not artenusate (100 muM), stimulated insulin release from pancreatic islets in vitvo.3 Macroscopic K-ATP currents were studied in inside-out patches excised from Xenopus oocytes expressing cloned K-ATP channels.4 Mefloquine (IC50 similar to3 muM), quinine (IC50 similar to3 muM), and chloroquine inhibited the pancreatic beta -cell type of KATP channel Kir6.2/SUR1. Artenusate (100 muM) was without effect.5 Mefloquine and quinine also blocked a truncated form of Kir6.2 (Kir6.2 Delta C36) when expressed in the absence of SUR1. The extent of block was similar to that observed for Kir6.2/SUR1 currents.6 Our results suggest that inhibition of the beta -cell K-ATP channel accounts for the ability of quinoline-based antimalarial drugs to stimulate insulin secretion, and thereby produce hypoglycaemia.7 The results also indicate that quinoline-based antimalarial agents inhibit K-ATP channels by interaction with the Kir6.2 subunit. This subunit is common to beta -cell, neuronal, cardiac, skeletal muscle, and some smooth muscle K-ATP channels suggesting that K-ATP channel inhibition may contribute to the other side effects of these drugs, which include cardiac conduction abnormalities and neuropsychiatric disturbances.