關鍵詞：慢肌肉纖維(Slow muscle fiber)；咖啡因攣縮(Caffeine contracture)；鈣離子流(Calcium flux)；異博定(Verapamil)；釓(Gadolinium)；非損傷微測技術(non-invasively using ion-selective vibrating microelectrodes， MIFE)。

參考文獻：Lana Shabala, et al. J Membrane Biol, 2008, 221: 7–13

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In this work, we tested whether L-type Ca²⁺ channels are involved in the increase of caffeine-evoked tension in frog slow muscle fibers. Simultaneous net Ca²⁺ fluxes and changes in muscle tension were measured in the presence of caffeine. Isometric tension was recorded by a mechanoelectrical transducer, and net fluxes of Ca²⁺ were measured noninvasively using ion-selective vibrating microelectrodes. We show that the timing of changes in net fluxes and muscle tension coincided, suggesting interdependence of the two processes. The effects of Ca²⁺ channel blockers (verapamil and gadolinium) were explored using 6 mM caffeine; both significantly reduced the action of caffeine on tension and on calcium fluxes. Both caffeineevoked Ca²⁺ leak and muscle tension were reduced by 75% in the presence of 100 lM GdCl₃, which also caused a 92% inhibition of net Ca²⁺ fluxes in the steady-state condition. Application of 10 lM verapamil to the bath led to 30% and 52% reductions in the Ca²⁺ leak caused by the presence of caffeine for the peak and steady-state values of net Ca²⁺ fluxes, respectively. Verapamil (10 lM) caused a 30% reduction in the maximum values of caffeine-evoked muscle tension. Gd³⁺ was a more potent inhibitor than verapamil. In conclusion, L-type Ca²⁺ channels appear to play the initial role of trigger in the rather complex mechanism of slow fiber contraction, the latter process being mediated by both positive Ca²⁺-induced Ca²⁺ release and negative (Ca²⁺ removal from cytosol) feedback loops.