Abstract. Effects of KRN4884 (5-amino-N-[2-(2-chlorophenyl)ethyl]-N'-cyano-3-pyridinecarboxamidine), a novel K + channel opener, on ionic currents were examined in rabbit femoral arterial myocytes (RFAMs). Under whole-cell clamp conditions where cells were superfused with 5.9 mM K + bathing solution, KRN4884 elicited an outward current at -30 mV. KRN4884-induced current had a reversal potential of -78 mV and was abolished by application of glibenclamide (glib). KRN4884 was approximately 43 times more potent than levcromakalim in activating an ATP-sensitive K + current (I K-ATP ). On the other hand, KRN4884 affected neither voltage-dependent Ca 2+ nor delayed rectifier K + channel currents. In the inside-out patch clamp configuration where cells were superfused with the symmetrical 140 mM K + solution, KRN4884 activated 47 pS K + channels in the presence of adenosine diphosphate. Similar 47 pS K + channels, which were reversibly inhibited by glib, were recorded under outside-out patch conditions. Using RT-PCR analysis, we found that inward rectifier K channel 6.1 (Kir6.1) and sulfonylurea 2B (SUR2B) transcripts were predominantly expressed in rabbit femoral artery. These results indicate that KRN4884 potently activates I K-ATP in RFAMs. The KRN4884-sensitive 47 pS K + channel activity underlying I K-ATP is a vascular type K ATP channel consisting of Kir6.1 and SUR2B and has similar characteristics to those of ATP-sensitive K + channels activated by K + channel openers in other types of smooth muscles.