Wu J R, Zhou Z, Bittar E E
Department of Physiology, University of Wisconsin, Madison 53706.
Biochim Biophys Acta. 1992 Nov 23;1112(1):99-104. doi: 10.1016/0005-2736(92)90259-o.
The hypothesis that chloramine-T stimulates the basal Na+ efflux in barnacle fibers as the result of the entry of trigger Ca2+ into the myoplasm from the bathing medium was examined in this study. Two reasons for doing so can be given. One is that the oxidant is known to abolish inactivation in sodium and potassium channels. The other is that L-type Ca2+ channels are present in barnacle fibers, and an increase in internal free Ca2+ in these fibers is known to stimulate the Na+ efflux, particularly in ouabain-poisoned fibers. The results of the experiments are as follows: (i) Chloramine-T exerts a biphasic effect on the Na+ efflux: inhibition is followed by stimulation, the threshold concentration being 10(-5) M. This is also found to be the threshold concentration for shortening of these fibers. (ii) The kinetics of the inhibitory effect resemble those of ouabain. (iii) Ouabain is without effect on the stimulatory phase caused by chloramine-T. (iv) Application of chloramine-T after the full effect of 10(-4) M-ouabain is reached elicits solely a stimulatory response. (v) The dose-response curves for the stimulatory action of chloramine-T in unpoisoned and ouabain-poisoned fibers are alike except that the threshold concentration is less than 10(-5) M in poisoned fibers. (vi) Basal light emission from unpoisoned and ouabain-poisoned fibers loaded with the photoprotein, aequorin, some 60 min beforehand increases as soon as they are exposed to 10(-4) M chloramine-T. The response recorded in unpoisoned fibers is monophasic and usually transitory, whereas it is multiphasic and usually sustained in ouabain-poisoned fibers. (vii) The dose-response curve for chloramine-T shows a shift to the left in poisoned fibers. (viii) The magnitude of the rise in light emission depends on the external Ca2+ concentration. A rise fails to take place in the nominal absence of external Ca2+. Taken together, these results support the above hypothesis that chloramine-T causes the entry of trigger Ca2+ into the myoplasm from the outside and provide evidence that stimulation of the Na+ efflux is associated not only with this event but also with a reduced Na+ gradient resulting from inhibition of the membrane Na+/K(+)-ATPase system by the oxidant. Thus, the suggestion put forward is that this oxidant promotes reverse Na+/Ca2+ exchange and is able to exert multiple effects on membrane transport.
氯胺 - T刺激藤壶纤维中的基础Na⁺外流，是由于触发Ca²⁺从浴液介质进入肌质的结果。这样做有两个原因。一是已知该氧化剂可消除钠通道和钾通道的失活。另一个原因是藤壶纤维中存在L型Ca²⁺通道，并且已知这些纤维中内部游离Ca²⁺的增加会刺激Na⁺外流，特别是在哇巴因中毒的纤维中。实验结果如下：(i)氯胺 - T对Na⁺外流产生双相作用：先是抑制，随后是刺激，阈值浓度为10⁻⁵M。这也是这些纤维缩短的阈值浓度。(ii)抑制作用的动力学类似于哇巴因。(iii)哇巴因对氯胺 - T引起的刺激阶段没有影响。(iv)在达到10⁻⁴M哇巴因的完全作用后应用氯胺 - T仅引发刺激反应。(v)氯胺 - T在未中毒和哇巴因中毒纤维中的刺激作用的剂量 - 反应曲线相似，只是中毒纤维中的阈值浓度小于10⁻⁵M。(vi)预先约60分钟加载光蛋白水母发光蛋白的未中毒和哇巴因中毒纤维，一旦暴露于10⁻⁴M氯胺 - T，基础发光就会增加。在未中毒纤维中记录到的反应是单相的且通常是短暂的，而在哇巴因中毒纤维中则是多相的且通常是持续的。(vii)氯胺 - T的剂量 - 反应曲线在中毒纤维中向左移动。(viii)发光增加的幅度取决于外部Ca²⁺浓度。在名义上没有外部Ca²⁺的情况下不会出现增加。综上所述，这些结果支持上述假设，即氯胺 - T导致触发Ca²⁺从外部进入肌质，并提供证据表明Na⁺外流的刺激不仅与此事件相关，还与氧化剂抑制膜Na⁺/K⁺ - ATP酶系统导致的Na⁺梯度降低有关。因此，所提出的建议是，这种氧化剂促进反向Na⁺/Ca²⁺交换，并能够对膜转运产生多种影响。
