The potassium current underlying delayed rectification in cat ventricular muscle.

1. Outward currents in cat ventricular fibres have been studied using the single sucrose gap method. The time dependent outward currents can be separated into a fast component, I(K), and a slow component, I(x). The voltage dependence of the I(K) time constant was bell-shaped, being about 150 msec at -90 mV, 500 msec at -25 mV and 300 msec at +30 mV. The combination of much faster time constants and larger amplitudes relative to I(x) allowed the estimation of I(K) amplitude, but not time course, from semilog plots of membrane currents accompanying 2 sec depolarizations.2. The ;steady-state' outward current at 2 sec (I(ss)) was separated into time independent background current (I(bg)) and time dependent I(K). The activation threshold for I(K) was about -50 mV and its amplitude increased steeply between -30 and +10 mV. The ratio of I(bg) to I(K) was about 1 between -30 and +30 mV.3. The current-voltage relations of I(ss) and I(bg) showed inward going rectification but negative slope regions were not observed. Raising the external K concentration from 3 to 10, 20 and 30 mM increased conductance and induced ;cross-overs' in the current-voltage relations. Increases in conductance were offset by the reductions in driving force, i.e. currents at plateau potentials were not larger in high K solutions.4. K accumulation occurs in response to prolonged membrane depolarization but conductance rather than accumulation appears to be responsible for the slowly rising outward current, I(x). However, the accumulation which takes place during the activation of I(x) may preclude an accurate determination of its time course and reversal potential.5. The potential at which outward I(K) tails declined to zero was strongly dependent on external K concentration in the range 3-30 mM. Inward going I(K) tails were difficult to detect because control hyperpolarization from the resting potential triggered large inward time dependent currents. Evidence is presented suggesting that much of this time dependency is due to the depletion of extracellular K from regions of restricted diffusion.6. The steady-state activation variable (n(infinity)) of the I(K)-system had to be calculated from isochronic (300 msec activating pulses) activation relations and tau(n)s because shifts in V(K) due to K accumulation precluded complete activations. The shape of n(infinity) was sigmoid approaching 0 at -60 mV, 0.5 at -20 mV and 1 at +20 mV.7. The fully activated current-voltage relation of I(K) displayed inward going rectification.8. It is concluded that there are strong similarities between I(K) in ventricular muscle and i(x1) in Purkinje fibres. Possible counterparts in frog atrial muscle include the currents labelled I(1) and i(x.slow).