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• W2000262972 abstract "Patients with congenital long QT syndrome may develop arrhythmias under conditions of increased sympathetic tone. We have addressed whether some of the beta-adrenoceptor blockers commonly used to prevent the development of these arrhythmias could per se block the cardiac HERG (Human Ether-a-go-go-Related Gene) potassium channels, which would be a most unwanted side effect. HERG potassium channels were heterologously expressed in Xenopus oocytes and the currents measured by two-electrode-voltage-clamp technique. Propranolol caused a concentration-dependent inhibition of HERG current with an IC50 value of 81 microM at -10 mV. When HERG was co-expressed with the accessory subunit KCNE2, an IC50 value of 52 microM was determined. The block by propranolol was voltage-dependent, but it did not change the HERG channel deactivation kinetics. The propranolol analogue ICI118551 ((+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol hydrochloride) blocked the HERG channel with similar affinity, whereas the beta1-receptor antagonists metoprolol and atenolol showed weak effects. Further, the four compounds blocked HERG channels expressed in a mammalian HEK293 cell line. These data showed that HERG blockade by beta-adrenoceptor blockers occurred only at high micromolar concentrations, which are significantly above the recently established safe margin of 100 (Redfern et al., 2003)." @default.
• W2000262972 created "2016-06-24" @default.
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• W2000262972 date "2005-01-26" @default.
• W2000262972 modified "2023-10-18" @default.
• W2000262972 title "Effect of β‐Adrenoceptor Blockers on HumanEther‐a‐go‐go‐Related Gene (HERG) Potassium Channels" @default.
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• W2000262972 doi "https://doi.org/10.1111/j.1742-7843.2005.pto960206.x" @default.
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