Puppi A, Szekeres S, Dely M
Central Laboratory of Animal Research, University Medical School, Pecs, Hungary.
Acta Physiol Hung. 1990;75(3):253-9.
Analyzing the mechanisms of redox-modulation of the excitatory-contractory process, recently the amplitude of K(+)-contractures, tissue redox-state potential and electrical burst activity were simultaneously measured in the rectus abdominis muscle of the frog (Rana esculenta) following oxidant (thionine) and reductant (ascorbate) treatments. Pretreatment with oxidant in parallel with the increment of redox-state potential increased, while pretreatment with reductant, parallel with the decrement of redox-state potential decreased significantly both the amplitudes of K(+)-contractures and the electrical burst activity. The main mechanisms of action of this phenomenon, at least of the phasic portion, in all probability is the increase of intracellular quotient of the ionized/bound calcium after oxidizing, but a decrease of this quotient following reducing shifts. In the case of tonic portion an increase of Ca2(+)-influx through the Na(+)-Ca2(+)-exchange diffusion mechanisms seems feasible. Other mechanisms are also discussed. Hence, the mechanism of K(+)-contractures is under the control of tissue redox-state potential as well.
在分析兴奋 - 收缩过程的氧化还原调节机制时，最近在对青蛙（食用蛙）的腹直肌进行氧化剂（硫堇）和还原剂（抗坏血酸盐）处理后，同时测量了钾离子收缩幅度、组织氧化还原状态电位和电爆发放活动。氧化剂预处理伴随着氧化还原状态电位的升高，钾离子收缩幅度增加；而还原剂预处理伴随着氧化还原状态电位的降低，钾离子收缩幅度和电爆发放活动均显著降低。这种现象（至少是其相位部分）的主要作用机制很可能是氧化后细胞内游离/结合钙的商增加，但还原后该商减少。对于紧张部分，通过钠 - 钙交换扩散机制增加钙离子内流似乎是可行的。还讨论了其他机制。因此，钾离子收缩的机制也受组织氧化还原状态电位的控制。
