Characterization of delayed rectifier K+ currents in rabbit coronary artery cells near resting membrane potential.

Previous studies have suggested that delayed rectifier K+ (Kdr) channels contribute to the control of membrane potential in vascular smooth muscle. To explore this hypothesis further, we investigated the characteristics of Kdr channels in the negative voltage range in the rabbit coronary artery. The Kdr channel blocker 4-aminopyridine (1 mM) contracted intact vessels and depolarized them from -52 to -37 mV, suggesting that these channels significantly contribute to the maintenance of resting membrane potential. In contrast, the ATP-sensitive K+ channel blocker glybenclamide (3 microM) had little effect on resting tone and did not alter the contraction elicited with 4-aminopyridine. K+ currents in isolated cells were then investigated by using whole-cell patch-clamp techniques. Increasing extracellular K+ concentration ([K+]o) from 5 to 135 mM resulted in the appearance of large inward currents at potentials between -60 and 0 mV. The voltage dependence of conductance for inward K+ currents was steeper and shifted toward more negative potentials when compared with outward K+ currents in 5 mM [K+]o solution. Various blockers of Kdr channels, i.e., 4-aminopyridine (3 mM), phencyclidine (0.1 mM), and intracellular tetraethylammonium (10 mM), nearly abolished currents in high [K+]o solution. In contrast, Ba2+ (0.1 mM) was without effect. These results suggest that the inward currents detected at potentials between -60 and 0 mV in high [K+]o solution are Kdr currents. Our results suggest that Kdr channels physiologically contribute to the control of membrane potential in the rabbit coronary artery.