Hoey A, Harrison S M, Boyett M R, Ravens U
Institute of Pharmacology, University of Essen, Germany.
Pharmacol Toxicol. 1994 Dec;75(6):356-65. doi: 10.1111/j.1600-0773.1994.tb00375.x.
The effects of the Anemonia sulcata toxin ATX II on action potentials and contractility of isolated papillary muscles and single myocytes from rat and guinea-pig hearts have been studied. ATX II prolonged the action potential in both rat and guinea-pig papillary muscle. Although it produced a positive inotropic effect in guinea-pig papillary muscle, it failed to do so in rat papillary muscle. However, in single rat and guinea-pig ventricular cells, it both prolonged the action potential and had a positive inotropic effect. We suggest that ATX II does not cause a positive inotropic effect in rat papillary muscle, because it induces Ca2+ overload. In single cells the positive inotropic effect was reduced by approximately 50% when the contractions were triggered by voltage clamp pulses of constant duration rather than by action potentials. This suggests that the inotropic effect of ATX II is in part the result of the prolongation of the action potential. The intracellular Na+ activity (a(i)Na) in single ventricular cells was measured with the Na(+)-sensitive fluorescent dye SBFI. After exposure of the cells to ATX II, a(i)Na was increased by a maximum of 1.9 +/- 0.3 and 2.2 +/- 0.3 mM in rat and guinea-pig cells, respectively. It is suggested that the positive inotropic effect of ATX II is also in part the result of the rise in a(i)Na.
研究了沟海葵毒素ATX II对大鼠和豚鼠心脏分离乳头肌及单个心肌细胞动作电位和收缩性的影响。ATX II使大鼠和豚鼠乳头肌的动作电位延长。虽然它对豚鼠乳头肌产生正性肌力作用，但对大鼠乳头肌却未产生此作用。然而，在大鼠和豚鼠单个心室细胞中，它既延长动作电位又具有正性肌力作用。我们认为ATX II在大鼠乳头肌中不产生正性肌力作用，是因为它诱导了Ca2+超载。在单个细胞中，当收缩由恒定持续时间的电压钳脉冲而非动作电位触发时，正性肌力作用降低了约50%。这表明ATX II的正性肌力作用部分是动作电位延长的结果。用钠敏感荧光染料SBFI测量单个心室细胞内的钠活性（a(i)Na）。细胞暴露于ATX II后，大鼠和豚鼠细胞中的a(i)Na分别最多增加1.9±0.3和2.2±0.3 mM。提示ATX II的正性肌力作用部分也是a(i)Na升高的结果。
