INWARD RECTIFIER K-MUSCLE CELLS FROM RAT CORONARY-ARTERIES - BLOCK BYMG2+, CA2+, AND BA2+( CURRENTS IN SMOOTH)

Inward rectifier K+ channels have been implicated in the control of me mbrane potential and external K+-induced dilations of small coronary a rteries. To identify and characterize inward rectifier K+ currents in coronary artery smooth muscle, whole cell K+ currents in smooth muscle cells enzymatically isolated from rat coronary (septal) arteries (dia meters, 100-150 mu m) were measured in the conventional and perforated configurations of the patch-clamp technique. Ba2+-sensitive, whole ce ll K+ current-voltage relationships exhibited inward rectification. Bl ockers of Ca2+-activated K+ channels (1 mM tetraethylammonium ion), AT P-sensitive K+ channels (10 mu M glibenclamide), and voltage-dependent K+ channels (1 mM 4-aminopyridine) in smooth muscle did not affect in ward rectifier K+ currents. The nonselective K+ channel inhibitor phen cyclidine (100 mu M) reduced inward rectifier K+ currents by similar t o 50%. External Ba2+ reduced inward currents, with membrane potential hyperpolarization increasing inhibition. The half-inhibition constant for Ba2+ was 2.1 mu M at -60 mV, decreasing e-fold for a 25-mV hyperpo larization. External Cs+ also blocked inward rectifier K+ currents, wi th the half-inhibition constant for Cs+ of 2.9 mM at -60 mV. External Ca2+ and Mg2+ reduced inward rectifier K+ currents. At -60 mV, Ca2+ an d Mg2+ (1 mM) reduced inward currents by 33 and 21%, respectively. Inw ard rectification was not affected by dialysis of the cell's interior with a nominally Ca2+- and Mg2+-free solution. These findings indicate that inward rectifier K+ channels exist in coronary artery smooth mus cle and that Ba2+ may be a useful probe for the functional role of inw ard rectifier K+ channels in coronary arteries.