Be. Robertson et al., INWARD RECTIFIER K-MUSCLE CELLS FROM RAT CORONARY-ARTERIES - BLOCK BYMG2+, CA2+, AND BA2+( CURRENTS IN SMOOTH), American journal of physiology. Heart and circulatory physiology, 40(2), 1996, pp. 696-705
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.