Suh C K, Park S R
Department of Physiology, Inha University College of Medicine, Inchon, Korea.
Yonsei Med J. 1993 Dec;34(4):311-20. doi: 10.3349/ymj.1993.34.4.311.
Ryanodine has different effects on the contractility of rat and guinea pig ventricular muscle. Thus we investigated the effect of ryanodine on the intracellular Ca2+ and Na+ activities of the rat and guinea pig ventricular myocytes with two specific aims; whether there are any differences in intracellular Na+ activities between rat and guinea pig ventricular muscle cells, and if any, how the differences in intracellular Na+ activities are related to the effect of Na(+)-Ca2+ exchange on the action potential configuration and excitation-contraction coupling of the rat and guinea pig ventricular myocytes. Ryanodine (10(-7) M) diminished the slow repolarization phase of the rat ventricular action potential while the duration of the rapid repolarization phase increased. Ryanodine (10(-7) M) significantly increased the plateau of the action potential. At the steady state of 0.2 cps, intracellular Na+ activities (aiNa) of the rat and guinea pig ventricular myocytes were 8.7 +/- 5.2 mM (n = 16, 4 rats) and 10.0 +/- 4.1 mM (n = 25, 7 guinea pigs) respectively, but there were no statistically significant differences. The contractility of the rat ventricular muscle nearly disappeared due to ryanodine (10(-7) M) with little changes in aiNa. Monensin (10 mM) not only increased the resting tension but also remarkably increased aiNa from 2.0 mM to 20 mM. Ryanodine (10(-7) M) continuously decreased aiNa of the guinea pig ventricular muscle after the contraction ceased to decrease. Monensin increased the contractility as well as aiNa. These results suggest that the contractility of rat and guinea pig ventricular myocytes is determined by the change in the action of the Na(+)-Ca2+ exchange mechanism depending upon the plateau of action potential and the intracellular Na+ and Ca2+ activities. So ryanodine could decreases the contractility via its effect on Na(+)-Ca2+ exchange transport which could be one of possible mechanisms of negative inotropism by ryanodine.
ryanodine对大鼠和豚鼠心室肌收缩性有不同影响。因此，我们研究了ryanodine对大鼠和豚鼠心室肌细胞内Ca2+和Na+活性的影响，有两个特定目的：大鼠和豚鼠心室肌细胞内Na+活性是否存在差异，若存在差异，细胞内Na+活性的差异如何与Na(+)-Ca2+交换对大鼠和豚鼠心室肌细胞动作电位形态及兴奋-收缩偶联的影响相关。ryanodine（10(-7) M）使大鼠心室动作电位的缓慢复极化阶段缩短，而快速复极化阶段的持续时间增加。ryanodine（10(-7) M）显著增加了动作电位的平台期。在0.2 cps的稳态下，大鼠和豚鼠心室肌细胞的细胞内Na+活性（aiNa）分别为8.7±5.2 mM（n = 16，4只大鼠）和10.0±4.1 mM（n = 25，7只豚鼠），但无统计学显著差异。ryanodine（10(-7) M）使大鼠心室肌收缩性几乎消失，而aiNa变化不大。莫能菌素（10 mM）不仅增加了静息张力，还使aiNa从2.0 mM显著增加到20 mM。在收缩停止下降后，ryanodine（10(-7) M）持续降低豚鼠心室肌的aiNa。莫能菌素增加了收缩性以及aiNa。这些结果表明，大鼠和豚鼠心室肌细胞的收缩性取决于Na(+)-Ca2+交换机制的作用变化，该变化取决于动作电位的平台期以及细胞内Na+和Ca2+活性。因此，ryanodine可通过其对Na(+)-Ca2+交换转运的影响降低收缩性，这可能是ryanodine产生负性肌力作用的一种可能机制。
