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Abstract
High-conductance Ca(2+)-activated K+ channels from rat skeletal muscle were incorporated
into planar lipid bilayers, and the channel kinetics were studied with a high internal
Ca2+ concentration (Cai). Raising the Cai is known to increase the channel open probability.
This effect is due to an increases in openings frequency and duration, and saturates
at a Cai around 100 microM. Raising the Cai also increases the occurrence of less
frequent but very long (> 5 s) shut events. The mechanism underlying this slow kinetic
process was studied. Raising Cai above 100 microM does not further increase the frequency
of the long shut events. This was not consistent with the hypothesis that the long
closures result from a classical channel-block mechanism induced by internal Ca2+.
The transmembrane voltage and the presence of K+ ions in the external compartment
both affect the slow kinetic process. A comparison of these effects with the properties
of the channel block induced by Ba2+ ions added to the internal compartment strongly
suggested that the long shut events are due to a contamination of the internal solutions
by Ba2+. This was confirmed by showing that a crown-ether compound that strongly chelates
Ba2+ completely suppresses the long shut events when added to the inner compartment.