A novel transient outward K+ current that exhibits inward-going rectificati
on (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 mu
mol/l Ba2+ or removal of external K+. The zero current potential shifted 5
1-53 mV/decade change in external K+. I-to.ir density was twofold greater i
n ventricular than in atrial myocytes, and biexponential inactivation occur
s in both types of myocytes. At -20 mV, the fast inactivation time constant
s were 7.7 +/- 1.8 and 6.1 +/- 1.2 ms and the slow inactivation time consta
nts 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, respec
tively). I-to.ir was detected in Na+-containing and Na+-free solutions and
was not blocked by 20 nmol/l saxitoxin. Action potential clamp revealed tha
t I-to.ir contributed an outward current that activated rapidly on depolari
zation and inactivated by early phase 2 in both tissues. Although it is wel
l known that 4-AP-sensitive transient outward current is absent in guinea p
ig, this Ba2+-sensitive and 4-AP-insensitive K+ current has been overlooked
.