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

Previous studies have suggested that delayed rectifier K+ (K-dr) channels contribute to the control of membrane potential in vascular smooth muscle. To explore this hypothesis further, we investigated the characteristics of K-dr channels in the negative voltage range in the rabbit coronary artery. The K-dr 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 mu M) 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+](0)) 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+](0) solution. Various blockers of K-dr channels, i.e., 4-aminopyridine (3 mM), phencyclidine (0.1 mM), and intracellular tetraethylammonium (10 mM), nearly abolished currents in high [K+](0) 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+](0) solution are K-dr currents. Our results suggest that K-dr channels physiologically contribute to the control of membrane potential in the rabbit coronary artery.