Rozenshtraukh L V, Saks V A, Undrovinas A I, Iuravichus I A, Iushmanova A V
Fiziol Zh SSSR Im I M Sechenova. 1977 May;63(5):681-8.
Creatine phosphate (10 and 20 mM) increased both the force of contraction and action potential duration in isolated frog heart strips. In concentration of 75 mM creatine phosphate increased the force of contraction during first minutes with its following decrease. Action potential duration was also increased during this period. These data suggest existence of receptory sites for creatine phosphate in the heart cells: the myofibrillar creatine phosphokinase system where creatine phosphate increases the force of contraction; and the cellular membranes where creatine phosphate decreases the rate of membrane repolarization. Dinitrofluorobenzene (1.5 mM) completely inhibited contraction of the heart strips and significantly decreased the duration and intensity of action potential. The data obtained are discussed from the view--point of existence of a creatine phosphate pathway for intracellular energy transport in the heart cells.
磷酸肌酸(10和20毫摩尔)可增强离体蛙心条的收缩力并延长动作电位持续时间。在75毫摩尔浓度时,磷酸肌酸在最初几分钟可增强收缩力,随后收缩力下降。在此期间动作电位持续时间也会延长。这些数据表明心肌细胞中存在磷酸肌酸的受体位点:肌原纤维磷酸肌酸激酶系统,磷酸肌酸在此处增强收缩力;以及细胞膜,磷酸肌酸在此处降低膜复极化速率。二硝基氟苯(1.5毫摩尔)完全抑制心条收缩,并显著缩短动作电位持续时间和降低动作电位强度。从心肌细胞内存在磷酸肌酸细胞内能量转运途径的角度对所得数据进行了讨论。