THE POTASSIUM CURRENT UNDERLYING DELAYED RECTIFICATION IN CAT VENTRICULAR MUSCLE

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Abstract
Outward currents in cat ventricular fibers were studied using the single sucrose gap method. The time-dependent outward currents can be separated into a fast component, IK, and a slow component, Ix. The voltage dependence of the IK time constant was bell-shaped, being about 150 ms at -90 mV, 500 ms at -25 mV and 300 ms at +30 mV. The combination of much faster time constants and larger amplitudes relative to Ix allowed the estimation of IK amplitude, but not time course, from semilog plots of membrane currents accompanying 2 s depolarizations. The steady-state outward current at 2 s (Iss) was separated into time-independent background current (Ibg) and time-dependent IK. The activation threshold for IK was about -50 mV and its amplitude increased steeply between -30 and +10 mV. The ratio of Ibg to IK was about 1 between -30 and +30 mV. The current-voltage relations of Iss and Ibg showed inward going rectification but negative slope regions were not observed. Raising the external K concentration from 3-10, 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. K accumulation occurs in response to prolonged membrane depolarization, but conductance rather than accumulation appears to be responsible for the slowly rising outward current, Ix. The accumulation which takes place during the activation of Ix may preclude an accurate determination of its time course and reversal potential. The potential at which outward IK tails declined to zero was strongly dependent on external K concentration in the range 3-30 mM. Inward going IK 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. The steady-state activation variable (n.infin.) of the IK-system had to be calculated from isochronic (300 ms activating pulses) activation relations to .tau.nS because shifts in VK [K velocity] due to K accumulation precluded complete activations. The shape of n.infin. was sigmoid approaching 0 at -60 mV, 0.5 at -20 mV and 1 at +20 mV. The fully activated current-voltage relation of IK displayed inward going rectification. There are strong similarities between IK in ventricular muscle and ix1 in Purkinje fibers. Possible counterparts in frog atrial muscle include the currents labeled I1 and ix.slow.