THERMAL-STRESS AND CA-INDEPENDENT CONTRACTILE ACTIVATION IN MAMMALIAN SKELETAL-MUSCLE FIBERS AT HIGH-TEMPERATURES

被引:51
作者
RANATUNGA, KW
机构
[1] Department of Physiology, Medical School, University of Bristol
基金
英国惠康基金;
关键词
D O I
10.1016/S0006-3495(94)80944-0
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Temperature dependence of the isometric tension was examined in chemically skinned, glycerinated, rabbit Psoas, muscle fibers immersed in relaxing solution (pH similar to 7.1 at 20 degrees C, pCa similar to 8, ionic strength 200 mM); the average rate of heating/cooling was 0.5-1 degrees C/s. The resting tension increased reversibly with temperature (5-42 degrees C); the tension increase was slight in warming to similar to 25 degrees C (a linear thermal contraction, -alpha, of similar to 0.1%/degrees C) but became more pronounced above similar to 30 degrees C (similar behavior was seen in intact rat muscle fibers). The extra tension rise at the high temperatures was depressed in acidic pH and in the presence of 10 mM inorganic phosphate; it was absent in rigor fibers in which the tension decreased with heating (a linear thermal expansion, alpha, of similar to 4 x 10(-5)/degrees C). Below similar to 20 degrees C, the tension response after a similar to 1% length increase (complete <0.5 ms) consisted of a fast decay (similar to 150.s(-1) at 20 degrees C) and a slow decay (similar to 10.s(-1)) of tension. The rate of fast decay increased with temperature (Q(10) similar to 2.4); at 35-40 degrees C, it was similar to 800.s(-1), and it was followed by a delayed tension rise (stretch-activation) at 30-40.s(-1). The linear rise of passive tension in warming to similar to 25 degrees C may be due to increase of thermal stress in titin (connectin)myosin composite filament, whereas the extra tension above similar to 30 degrees C may arise from cycling cross-bridges; based on previous findings from regulated actomyosin in solution (Fuchs, 1975), it is suggested that heating reversibly inactivates the troponin-tropomyosin control mechanism and leads to Ca-independent thin filament activation at high temperatures. Additionally, we propose that the heating-induced increase of endo-sarcomeric stress within titin-myosin composite filament makes the crossbridge mechanism stretch-sensitive at high temperatures.
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页码:1531 / 1541
页数:11
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