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Biophys J, September 1998, p. 1271-1286, Vol. 75, No. 3
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106 USA
Ca2+ entry under resting conditions may be
important for contraction of vascular smooth muscle, but little is
known about the mechanisms involved. Ca2+ leakage was
studied in the A7r5 smooth muscle-derived cell line by patch-clamp
techniques. Two channels that could mediate calcium influx at resting
membrane potentials were characterized. In 110 mM Ba2+, one
channel had a slope conductance of 6.0 ± 0.6 pS and an
extrapolated reversal potential of +41 ± 13 mV (mean ± SD,
n = 8). The current rectified strongly, with no
detectable outward current, even at +90 mV. Channel gating was voltage
independent. A second type of channel had a linear current-voltage
relationship, a slope conductance of 17.0 ± 3.2 pS, and a
reversal potential of +7 ± 4 mV (n = 9). The
open probability increased e-fold per 44 ± 10 mV
depolarization (n = 5). Both channels were also
observed in 110 mM Ca2+. Noise analysis of whole-cell
currents indicates that ~100 6-pS channels and 30 17-pS channels are
open per cell. These 6-pS and 17-pS channels may contribute to resting
calcium entry in vascular smooth muscle cells.
Biophys J, September 1998, p. 1271-1286, Vol. 75, No. 3
© 1998 by the Biophysical Society 0006-3495/98/09/1271/16 $2.00
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