AJP - Cell Physiology, Vol 252, Issue 2 C190-C196, Copyright © 1987 by American Physiological Society
Sodium permeability of frog skeletal muscle in absence and presence of veratridine
L. C. McKinney and R. W. Ratzlaff
The effect of veratridine on the Na permeability of frog sartorius muscle
was studied by means of ion flux measurements using radiolabeled sodium.
Veratridine increases Na influx in a dose-dependent manner (apparent Kd =
160 +/- 7 microM when Vm congruent to -40 mV). The increase can be
completely inhibited by tetrodotoxin (TTX) (apparent Ki = 8 +/- 2 nM),
indicating that all veratridine-induced Na influx occurs via sodium
channels. The time constant for the rate of onset of veratridine action is
1 h. Raising external pH one unit to 8.3 causes the rate of action of
veratridine and the final level of Na influx to increase. The apparent Kd
for veratridine depends on membrane voltage. Values obtained in 2.5 and 5
mM K Ringer (Vm congruent to -95 and -80 mV) were 579 +/- 279 and 35 +/- 8
microM, respectively. Veratridine-induced Na influx obeys the Goldman
constant field flux equation and when veratridine concentration is 1 mM,
sodium permeability is 1.5 X 10(-7) cm/s. This is much less than the
maximum PNa (1.6 X 10(-3) cm/s) obtained from voltage-clamp measurements of
peak Na conductance. Mg (52 mM) inhibits veratridine-induced influx by
about half. Aspects of resting Na influx in the absence of veratridine (but
in the presence of ouabain) were also characterized. Steady-state Na influx
is unaffected by tetrodotoxin over the voltage range -90-0 mV, suggesting
that no sodium channels are open in the resting state. Na influx is also
insensitive to curare. It is linearly dependent on external sodium and
larger at more negative membrane potentials.
