Induction and removal of inward-going rectification in sheep cardiac Purkinje fibres.
1. In sheep cardiac Purkinje fibres superfused with K-free, Na-free medium, the membrane potential can be stable either at a low negative level (-50 mV) or at a high negative level (-100 mV). The mechanism underlying the existence of these two stable potential levels was investigated using the two-micro-electrode voltage-clamp technique.2. By applying a voltage clamp of a certain duration at an appropriate level the membrane potential could be shifted from one stable level to the other. The shift was observed in Cl-free medium, excluding a redistribution of Cl as a possible explanation.3. Currents during and following a voltage step and their change with amplitude and duration of the voltage step could not be explained on the basis of depletion or accumulation of K ions in the narrow extracellular clefts.4. Instantaneous currents determined from the high negative resting level showed a high conductance and a pronounced inward rectification, while measurements from the low negative resting level indicated a low conductance and absence of inward rectification. The steady-state current-voltage relation was dependent on the holding potential and showed memory or hysteresis.5. Estimation of the conductance by superimposed short voltage-clamp pulses showed an increase in conductance during a hyperpolarizing clamp from the low negative level and a decrease in conductance during a depolarizing clamp from the high negative level. The time-dependent current during a hyperpolarizing clamp from the low negative level reversed direction at a potential level corresponding to E(K), assuming a cleft K concentration of about 1 mM. In the presence of 0.1 mM-Ba the time-dependent current was abolished.6. The results suggest that the shift between the two stable levels is due to a time-dependent conductance change in the K inward rectifier channel, i(K1). The existence of memory excludes activation or de-activation only depending on the voltage gradient. Interaction of extracellular K ions with a site in the membrane is proposed as the activating mechanism.
D000818:Animals; D001464:Barium / Q000494:pharmacology; D004553:Electric Conductivity; D006329:Heart Conduction System / Q000502:physiology*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D011690:Purkinje Fibers / Q000502:physiology*; D012756:Sheep / Q000502:physiology; D012964:Sodium / Q000494:pharmacology
D007473:Ion Channels; D001464:Barium; D012964:Sodium; D011188:Potassium