Zacharová D, Lipská E, Hencek M, Hochmannová J, Sajter V
Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Bratislava.
Gen Physiol Biophys. 1993 Dec;12(6):543-77.
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)
在螯虾(Astacus fluviatilis)完整肌纤维的电流钳制条件下以及内部灌注的肌纤维节段的电压钳制条件下,分别研究了儿茶酚胺对基本膜特性(包括标记离子通量)和收缩参数的影响;即在基于钙原理产生动作电位并激活张力的肌纤维中进行研究。肾上腺素和去甲肾上腺素(6×10⁻⁶ mol/L)均促进了由分级膜反应或锶全或无动作电位诱导的抽搐张力。未观察到异丙肾上腺素的作用。肾上腺素(6×10⁻⁶ - 6×10⁻⁵ mol/L)产生了正性肌力作用,该作用在2分钟时出现延迟,并在5分钟时达到最大值。收缩的激活和松弛速率增加,而潜伏期和阈值去极化降低。冲洗肾上腺素后,这些变化持续(数十分钟),这取决于肾上腺素的浓度和应用持续时间。静息电位和锶动作电位(Ca²⁺被Sr²⁺替代)不受影响,且肾上腺素促进了分级反应(从36.4±1 mV至40.0±2 mV;RP = 77.2±0.5 mV)。肾上腺素的正性肌力作用需要细胞外Ca²⁺离子的存在。在名义上无钙的溶液中或用Ni²⁺离子(1 mmol/L)阻断Ca²⁺内流后,电反应和收缩反应的降低可被肾上腺素缓解。当细胞外Ca²⁺离子浓度[Ca²⁺]₀从13.5 mmol/L降至3.4 mmol/L或添加Ni²⁺离子时,肾上腺素的正性肌力作用不再持续。在存在Ni²⁺离子的情况下,⁸⁹Sr²⁺离子的内流从24.2±4.7 pmol·cm⁻²·s⁻¹降至11.0±2.8 pmol·cm⁻²·s⁻¹,但在存在肾上腺素(6 μmol/L)时恢复至20.4±5.8 pmol·cm⁻²·s⁻¹。肾上腺素本身降低了⁸⁹Sr²⁺离子的内流,并延长了静息和受刺激纤维中流出的时间常数。肾上腺素的作用取决于从肌浆网中动员Ca²⁺离子。首先,尽管活性膜反应增加(普鲁卡因全或无动作电位),但在存在普鲁卡因(肌浆网钙释放通道阻断剂)的情况下,肾上腺素的正性肌力作用不存在;其次,肾上腺素加速了肌浆网对Ca离子的摄取,这通过肾上腺素缩短咖啡因挛缩后的恢复过程得以证明。通常,肾上腺素会增加膜钙电流;主要在较低去极化(-50至-20 mV)时。(摘要截断于400字)