Leite C M, Vassallo D V, Mill J G
Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, Brasil.
Braz J Med Biol Res. 1991;24(8):843-6.
Post-rest potentiated contractions have been reported to be more dependent on Ca2+ stored in intracellular sites than on transmembrane Ca2+ influx. The phenomenon was examined using toad ventricular strips contracting isometrically and superfused with Ringer solution. Toad ventricular strips did not present post-rest potentiation, a fact that may be explained by the reduced volume of the sarcoplasmic reticulum in the amphibian myocardium. Potentiated post-rest contractions were obtained after calcium influx blockade with 10 microM verapamil or 2 mM Mn2+ and the slow reduction of extracellular Ca2+ concentration obtained by slowly exchanging the bath fluid was accompanied by a progressive decrease of both steady-state and post-rest contractions. These data confirm the observations made on other species regarding the post-rest potentiation phenomenon and support the suggestion of the dependence of post-rest potentiation on activator calcium liberated from intracellular stores.
据报道,静息后增强收缩对细胞内储存的Ca2+的依赖性比对跨膜Ca2+内流的依赖性更大。使用等长收缩并灌注任氏液的蟾蜍心室肌条来研究该现象。蟾蜍心室肌条未出现静息后增强,这一事实可能由两栖类心肌肌浆网体积减小来解释。在用10微摩尔维拉帕米或2毫摩尔Mn2+阻断钙内流后获得了静息后增强收缩,并且通过缓慢更换浴液使细胞外Ca2+浓度缓慢降低,同时伴随着稳态收缩和静息后收缩的逐渐减少。这些数据证实了在其他物种上关于静息后增强现象的观察结果,并支持静息后增强依赖于从细胞内储存释放的激活钙的观点。