Abstract:
:The human ether-a-go-go-related gene (herg) encodes a K+ current (I(HERG)) which plays a fundamental role in heart excitability and in neurons by contributing to action potential repolarization and to spike-frequency adaptation, respectively. In this paper we show that I(HERG), recorded in neuroblastoma cells and guinea-pig ventricular myocytes, was reversibly inhibited by the K(ATP) channel blocker glibenclamide (IC50 = 74 microM). The voltage and use dependence of glibenclamide blockade were also evaluated. Another sulfonylurea, glimepiride, had less effective results in blocking I(HERG). The findings of this study are relevant to the interpretation of glibenclamide effects on cellular electrophysiology and suggest that oral antidiabetic therapy with sulfonylureas may contribute to iatrogenic QT prolongation and related arrhythmias.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Rosati B,Rocchetti M,Zaza A,Wanke Edoi
10.1016/s0014-5793(98)01444-6subject
Has Abstractpub_date
1998-11-27 00:00:00pages
125-30issue
1-2eissn
0014-5793issn
1873-3468pii
S0014-5793(98)01444-6journal_volume
440pub_type
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