Be. Robertson et Mt. Nelson, AMINOPYRIDINE INHIBITION AND VOLTAGE-DEPENDENCE OF K-MUSCLE CELLS FROM CEREBRAL-ARTERIES( CURRENTS IN SMOOTH), American journal of physiology. Cell physiology, 36(6), 1994, pp. 30001589-30001597
Voltage-dependent K+ currents were characterized using the patch-clamp
technique in smooth muscle cells isolated from rabbit cerebral (basil
ar) arteries. This study focused on the voltage dependence and the pha
rmacology of these K+ currents, since this information will be useful
for the investigation of the role of the voltage-dependent K+ channels
in arterial function. Currents through Ca2+-activated K+ (K-Ca) chann
els were minimized by buffering intracellular Ca2+ to low levels and b
y blockers (tetraethylammonium and iberiotoxin) of these channels. Mem
brane depolarization increased K+ currents, independent of changes in
the driving force for K+ movement. With 140 mM internal and external K
+, activation of K+ currents by membrane depolarization was half maxim
al at about -10 mV and increased as much as e-fold per 11 mV. Inactiva
tion also depended on voltage, with a midpoint at -44 mV. 3,4-Diaminop
yridine (3,4-DAP), 4-aminopyridine (4-AP), S-aminopyridine (3-AP), and
2-aminopyridine (2-AP) inhibited voltage-dependent K+ currents. At 0
mV, 3,4-DAP, 4-AP, 3-AP, and 2-AP (5 mM) inhibited the K+ currents by
84, 66, 36, and 8%, respectively. Phencyclidine (100 mu M) inhibited t
he current by 53% at 0 mV. Steady-state whole cell currents through th
ese channels were measured at physiological membrane potentials. At -4
0 mV, 4-AP (5 mM) reduced the steady-state outward current by 2.5 pA.
These results are consistent with the idea that voltage-dependent K+ c
hannels are involved in the regulation of the membrane potential of ar
terial smooth muscle.