MODULATION BY ADRENALINE OF ELECTROPHYSIOLOGICAL MEMBRANE PARAMETERS AND CONTRACTILITY IN INTACT AND INTERNALLY PERFUSED SINGLE MUSCLE-FIBERS OF THE CRAYFISH

(1) The effect of catecholamines on basic membrane characteristics (in cluding 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 cray fish Astacus fluviatilis; i.e. in muscle fibres which spike and activa te tension on calcium principle. (2) Both adrenaline and noradrenaline (6.10(-6) mol/l) facilitated twitch tension induced by graded membran e responses or strontium all-or-none spikes. No effect of isoprenaline was observed. (3) Adrenaline (6.10(-6) - 6.10(-5) mol/l) produced an inotropic effect, which appeared with a latency of 2 min and reached i ts maximum in 5 min. The rates of activation and relaxation of contrac tion were increased, whilst the latency and the threshold depolarizati on were decreased. The changes persisted (several tens of min) after w ashout of adrenaline, depending on concentration and duration of adren aline application. (4) 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; R P;= 77.2 +/- 0.5 mV). (5) Extracellular Ca2+ ions are required for the inotropic effect of adrenaline to occur. The decrease of electrical a nd contractile responses in nominal calcium-free solutions or after a blockade of Ca2+ influx by Ni2+, ions (1 mmol/l) was relieved by adren aline. The persistence of inotropic effect of adrenaline was absent, w hen the extracellular concentration of Ca2+ ions, [Ca2+](0) was decrea sed from 13.5 to 3.4 mmol/l or the Ni2+ ions were added. The influx Sr -89(2+) 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 t o 20.4 +/- 5.8 pmol.cm(-2).s(-1) in the presence of adrenaline (6 mu m ol/l). (6) Adrenaline itself decreased the influx, of Sr-89(2+) ions, and prolonged the time constant of efflux both in resting and stimulat ed fibres. (7) The effect of adrenaline is dependent on mobilization o f Ca2+ ions from the sarcoplasmic reticulum. First, the inotropic effe ct 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 act ive membrane response (all-or-none procaine action potential); second, adrenaline accelerated the uptake of Ca ions by SR as evidenced by sh ortening of the restitution processes after caffeine contractures by a drenaline. (8) Membrane calcium currents are increased by adrenaline a s a rule; mainly at lower depolarizations (-50 to -20 mV). All compone nts of the whole calcium conductance, which differ by time constants o f activation tau(M), and inactivation tau(h) (i.e. of the fast, the in termediate and the slow calcium conductance respectively) are increase d in the presence of adrenaline. The calcium conductance of the fast c omponent was increased by 31 +/- 6.3%, of the slow component by 132.2 +/- 27.6% and of the intermediate component by 101.5 +/- 20.9% (n = 22 , P = 0.01-0.001). The enhancement of calcium currents persisted after the withdrawal of adrenaline from the bathing solution. The time cons tants of activation, tau(M), were not significantly changed; the time constant of inactivation, tau(h) in the fast calcium channel was prolo nged.