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Cardiovascular Research 2001 49(4):790-797; doi:10.1016/S0008-6363(00)00306-0
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

The slow component of the delayed rectifier potassium current in undiseased human ventricular myocytes

László Virága, Norbert Iosta,d, Miklós Opincariub, Jenoó Szolnokyb, János Szécsib, Gábor Bogátsb, Pál Szenohradszkyc, András Varróa and Julius Gy. Pappa,d,*

aDepartment of Pharmacology and Pharmacotherapy, Albert Szent-Györgyi Medical University, Dóm tér 12, P.O. Box 427, H-6720 Szeged, Hungary
bDepartment of Cardiac Surgery, Albert Szent-Györgyi Medical University, Szeged, Hungary
cDepartment of Surgery, Albert Szent-Györgyi Medical University, Szeged, Hungary
dResearch Unit for Cardiovascular Pharmacology, Hungarian Academy of Sciences, Szeged, Hungary

* Corresponding author. Tel.: +36-62-545-681; fax: +36-62-544-565 papp{at}phcol.szote.u-szeged.hu

Objective: The purpose of this study was to investigate the properties of the slow component of the delayed rectifier potassium current (IKs) in myocytes isolated from undiseased human left ventricles. Methods: The whole-cell configuration of the patch-clamp technique was applied in 58 left ventricular myocytes from 15 hearts at 37°C. Nisoldipine (1 µM) was used to block inward calcium current (ICa) and E-4031 (1–5 µM) was applied to inhibit the rapid component of the delayed rectifier potassium current (IKr). Results: In 31 myocytes, an E-4031 insensitive, but L-735,821 and chromanol 293B sensitive, tail current was identified which was attributed to the slow component of IK (IKs). Activation of IKs was slow ({tau} = 903±101 ms at 50 mV, n = 14), but deactivation of the current was relatively rapid ({tau} = 122.4±11.7 ms at –40 mV, n = 19). The activation of IKs was voltage independent but its deactivation showed clear voltage dependence. The deactivation was faster at negative voltages (about 100 ms at –50 mV) and slower at depolarized potentials (about 300 ms at 0 mV). In six cells, the reversal potential was –81.6±2.8 mV on an average which is close to the K+ equilibrium potential suggesting K+ as the main charge carrier. Conclusion: In undiseased human ventricular myocytes, IKs exhibits slow activation and fast deactivation kinetics. Therefore, in humans IKs differs from that reported in guinea pig, and it best resembles IKs described in dog and rabbit ventricular myocytes.

KEYWORDS Cell culture/isolation; K-channel; Membrane currents; Myocytes; Ventricular arrhythmias


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