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1 Department of Medicine, Montreal Heart Institute and University of Montreal, Montreal, Quebec, Canada H3C 3J7; and 2 Department of Physiology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298
A novel transient outward K+
current that exhibits inward-going rectification
(Ito.ir) was identified in guinea pig atrial and
ventricular myocytes. Ito.ir was insensitive to
4-aminopyridine (4-AP) but was blocked by 200 µmol/l Ba2+
or removal of external K+. The zero current potential
shifted 51-53 mV/decade change in external K+.
Ito.ir density was twofold greater in
ventricular than in atrial myocytes, and biexponential inactivation
occurs in both types of myocytes. At
20 mV, the fast inactivation
time constants were 7.7 ± 1.8 and 6.1 ± 1.2 ms and the slow
inactivation time constants were 85.1 ± 14.8 and 77.3 ± 10.4 ms in ventricular and atrial cells, respectively. The midpoints
for steady-state inactivation were
36.4 ± 0.3 and
51.6 ± 0.4 mV, and recovery from inactivation was rapid near the resting
potential (time constants = 7.9 ± 1.9 and 8.8 ± 2.1 ms, respectively). Ito.ir was detected in
Na+-containing and Na+-free solutions and was
not blocked by 20 nmol/l saxitoxin. Action potential clamp revealed
that Ito.ir contributed an outward current that
activated rapidly on depolarization and inactivated by early phase 2 in
both tissues. Although it is well known that 4-AP-sensitive transient
outward current is absent in guinea pig, this
Ba2+-sensitive and 4-AP-insensitive K+ current
has been overlooked.
transient outward potassium current; whole cell patch clamp; repolarization; excitability; action potential configuration
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