B. Doepner, R. Koopmann, A. Knopp
Jul 1, 2001
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Journal
Naunyn-Schmiedeberg's Archives of Pharmacology
Abstract
Abstract. Ventricular myocytes of the mouse ventricle were voltage clamped with a patch-clamp technique in the whole-cell configuration. At depolarizing voltage pulses, these myocytes develop a large voltage-dependent K+ outward current. Application of the drug dibenzylamine (DBA) to the bath solution blocked the voltage-dependent K+ current. The concentration/response relationship for the peak current at +40 mV indicates a 1:1 binding of the drug to the receptor with a concentration of half maximum effect of 43.1 µmol/l. The block did not require activation of the channels by depolarizing pulses. At concentrations causing partial block (25 µmol/l), the block was independent of voltage. At the same concentration, DBA completely blocked the slow component of the recovery from inactivation (–80 mV) whereas steady-state inactivation was not altered. It is concluded that DBA is a novel blocker of the voltage-dependent K+ current in mouse cardiac myocytes which preferentially affects the current component generating the slow recovery from inactivation.