Mutungi Gabriel
Department of Physiology, University of Bristol, Bristol BS8 1TD, England.
J Muscle Res Cell Motil. 2003;24(1):65-75. doi: 10.1023/a:1024813505903.
The effects of adding either 25 mM inorganic phosphate (Pi) or its structural analogue arsenate (ASi) on both the maximum Ca2+ activated tension (Po) and passive muscle visco-elasticity (P2 tension) were investigated at 10 degrees C, using segments of single, chemically skinned rat muscle fibres. Whilst the results confirmed some previous findings on the effects of Pi on Po, they also showed that the addition of 25 mM ASi led to a large (approximately 50%) but completely reversible depression of Po in both the fast and slow twitch rat muscle fibres. Moreover, the depression of Po by ASi was greater at low than at high pH values. Examined in the presence of Dextran T-500, the passive tension and sarcomere length responses to a ramp stretch were found to be qualitatively and quantitatively similar to those previously reported in intact rat muscle fibres. Thus, the tension response to a ramp stretch, in the presence and absence of either 25 mM Pi or ASi, consisted of a viscous (P1), a visco-elastic (P2) and an elastic (P3) tension. However, the addition of either 25 mM Pi or ASi led to approximately 15-18% increase in the amplitude of the visco-elastic (P2) tension but had little or no effect on the amplitudes of the other two tension components (viscous, P1 and elastic, P3 tensions). Furthermore, neither compound significantly altered the relaxation rate of the passive muscle visco-elasticity (P2 tension). These results show that Po (arising from cycling cross-bridges) and passive muscle visco-elasticity (P2 tension) are affected differently by both Pi and ASi and suggest that they may not share a common structural basis. The possibility that passive muscle visco-elasticity (P2 tension) arises from the gap-(titin) filament (as suggested previously by Mutungi and Ranatunga, 1996b J Physiol 496: 827-837) and that Pi and ASi increase its amplitude by interacting with the PEVK region of the filament are discussed.
在10℃下，使用单个化学去皮大鼠肌肉纤维片段，研究了添加25 mM无机磷酸盐（Pi）或其结构类似物砷酸盐（ASi）对最大Ca2+激活张力（Po）和被动肌肉粘弹性（P2张力）的影响。虽然结果证实了一些先前关于Pi对Po影响的发现，但它们也表明，添加25 mM ASi会导致快速和慢速抽搐大鼠肌肉纤维中的Po大幅降低（约50%），但完全可逆。此外，ASi对Po的抑制在低pH值时比高pH值时更大。在存在葡聚糖T-500的情况下进行检查，发现对斜坡拉伸的被动张力和肌节长度反应在质量和数量上与先前在完整大鼠肌肉纤维中报道的相似。因此，在存在和不存在25 mM Pi或ASi的情况下，对斜坡拉伸的张力反应由粘性（P1）、粘弹性（P2）和弹性（P3）张力组成。然而，添加25 mM Pi或ASi会导致粘弹性（P2）张力的幅度增加约15-18%，但对其他两个张力成分（粘性，P1和弹性，P3张力）的幅度几乎没有影响。此外，两种化合物都没有显著改变被动肌肉粘弹性（P2张力）的松弛速率。这些结果表明，Po（由循环横桥产生）和被动肌肉粘弹性（P2张力）受Pi和ASi的影响不同，并表明它们可能没有共同的结构基础。讨论了被动肌肉粘弹性（P2张力）是否由间隙（肌联蛋白）细丝产生的可能性（如Mutungi和Ranatunga先前在1996年《生理学杂志》496：827-837中所建议的），以及Pi和ASi是否通过与细丝的PEVK区域相互作用来增加其幅度。
