Volume sensitive 36Cl fluxes in L6 myoblasts.

Efflux of 36Cl ions was followed in undifferentiated L6 myoblasts at rest and after exposure to hypotonic saline in order to test participation of the chloride exit in regulatory volume decrease mechanism. The efflux curve can be fitted at least with two time constants. After the hypotonic stress the slow rate constant increases almost threefold, from 0.021 +/- 0.019 min-1 normal saline to 0.060 +/- 0.019 min-1 in hypotonic solution.

Modulation by adrenaline of electrophysiological membrane parameters and contractility in intact and internally perfused single muscle fibres of the crayfish.

The effect of catecholamines on basic membrane characteristics (including labeled ionic fluxes) and contractile parameters was followed in current clamp and voltage clamp conditions in intact muscle fibres and internally perfused muscle fibre segments respectively of the crayfish Astacus fluviatilis; i.e. in muscle fibres which spike and activate tension on calcium principle. Both adrenaline and noradrenaline (6.10(-6) mol/l) facilitated twitch tension induced by graded membrane responses or strontium all-or-none spikes. No effect of isoprenaline was observed. Adrenaline (6.10(-6)-6.10(-5) mol/l) produced an inotropic effect, which appeared with a latency of 2 min and reached its maximum in 5 min. The rates of activation and relaxation of contraction were increased, whilst the latency and the threshold depolarization were decreased. The changes persisted (several tens of min) after washout of adrenaline, depending on concentration and duration of adrenaline application. The resting potential and the strontium spike (Ca2+ replaced with Sr2+) were not influenced and the graded responses were facilitated by adrenaline (from 36.4 +/- 1 mV to 40.0 +/- 2 mV; RP = 77.2 +/- 0.5 mV). Extracellular Ca2+ ions are required for the inotropic effect of adrenaline to occur. The decrease of electrical and contractile responses in nominal calcium-free solutions or after a blockade of Ca2+ influx by Ni2+ ions (1 mmol/l) was relieved by adrenaline. The persistence of inotropic effect of adrenaline was absent, when the extracellular concentration of Ca2+ ions, [Ca2+]0 was decreased from 13.5 to 3.4 mmol/l or the Ni2+ ions were added. The influx of 89Sr2+ ions was decreased in the presence of Ni2+ ions from 24.2 +/- 4.7 pmol.cm-2.s-1 to 11.0 +/- 2.8 pmol.cm-2.s-1, but restored to 20.4 +/- 5.8 pmol.cm-2.s-1 in the presence of adrenaline (6 mumol/l). Adrenaline itself decreased the influx of 89Sr2+ ions, and prolonged the time constant of efflux both in resting and stimulated fibres. The effect of adrenaline is dependent on mobilization of Ca2+ ions from the sarcoplasmic reticulum. First, the inotropic effect of adrenaline was absent in the presence of procaine (blockator of the Ca release channel of the SR), in spite of the increase of the active membrane response (all-or-none procaine action potential); second, adrenaline accelerated the uptake of Ca ions by SR as evidenced by shortening of the restitution processes after caffeine contractures by adrenaline. Membrane calcium currents are increased by adrenaline as a rule; mainly at lower depolarizations (-50 to -20 mV).(ABSTRACT TRUNCATED AT 400 WORDS)