The interaction of potassium with the activation of anomalous rectification in frog muscle membrane.

Abstract

SUMMARY1. Inward rectification of frog muscle membrane was analysed with the Vaseline gap method.2. Hyperpolarization, under voltage clamp, produced inward potassium currents, which had a component that activated with a time constant, TK* 3. The activation time constant TK of the inward potassium currents was voltage dependent. For a given external potassium concentration, the time constant was maximal for potentials near the potassium equilibrium potential, EK.4. The potassium chord conductance gK, had a sigmoidal voltage dependency, increasing initially e-fold per 11-6 mV of hyperpolarization.5. When the internal potassium concentration was fixed, raising external potassium induced a shift of the rK-V and the 9K-V relations in the positive direction along the voltage axis. That shift was comparable to the change in EK.6. No shift of the TK -V and the gK -V relations was observed when the internal potassium was reduced from 150 to 50 mm. 7. Changes of internal sodium concentration between 5 and 100 mm did not significantly effect the magnitude of inward rectification.

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

“…1978;Standen & Stanfield, 1978b) and Cs+ (Hagiwara et al 1976;Gay & Stanfield, 1977;Constanti & Galvan, 1983). The activation variable of this conductance shows V-EK dependence (Hagiwara et al 1976;Leech & Stanfield, 1981;Hestrin, 1981;Constanti & Galvan, 1983); that is it appears as if the conductance depends on the difference between the membrane and K+ equilibrium potentials, rather than on the membrane potential alone.…”

“…Part of the potentiating action of K+ undoubtedly occurs as a result of an increase in the driving force for inward K+ current, since the K+ equilibrium potential shifts in the depolarizing direction. It is possible that K+ also has a direct potentiating action on current flow through the inward rectifier, as occurs in skeletal muscle (Standen & Stanfield, 1978c;Hestrin, 1981;Leech & Stanfield, 1981) and cardiac Purkinje fibres (DiFrancesco, 1982).…”

“…For example Na+ ions increase the single-channel conductance of the inward rectifier in tunicate egg cell membranes (Fukushima, 1982) but are not themselves permeant. Potassium ions increase the conductance of the inward rectifier in skeletal muscle (Hestrin, 1981;Leech & Stanfield, 1981) and Purkinje fibres (DiFrancesco, 1982) and are also permeable. Thus although the data presented strongly suggest that both Na+ and K+ contribute directly to Ih, the results are not unambiguous.…”

“…The properties ofthe inward rectifier in muscle have since been examined in some detail (Hodgkin & Horowicz, 1959;Adrian & Freygang, 1962 a, b;Nakajima, Iwasaki & Obata, 1962;Almers, 1972;Standen & Stanfield, 1978a, b, 1980Hestrin, 1981) and it is known that the underlying conductance, which is relatively specific for K+ ions, increases with membrane potential hyperpolarization and varies with the extracellular K+ concentration as a function of the difference between the membrane and K+ equilibrium potentials (Hestrin, 1981;Leech & Stanfield, 1981). A similar conductance is present in a number of marine egg cell membranes (starfish: Hagiwara & Takahashi, 1974;sea-squirt: Miyazaki, Takahashi, Tsuda & Yoshii, 1974).…”

Intrinsic gating properties of a cloned G protein-activated inward rectifier K+ channel.

“…For example, the V1/2 -VK value for intrinsic gating of the background cardiac/~r channel is -7 mV (Kurachi, 1985;Saigusa and Matsuda, 1988;Ishihara et al, 1989;Oliva, Cohen, and Pennefather, 1990). For/~r channels in skeletal muscle fibers, the V1/2 -VK value is --25 mV in frog dorsal head semitendinosus muscle (Hestrin, 1981) and -11 mV in frog sartorius muscle (Leech and Standen, 1981). For the endothelial cell/~ channel, the value is -8 mV (Silver and DeCoursey, 1990).…”