首页> 美国卫生研究院文献>The Journal of Physiology >Evidence by calorimetry for an activation of sodium-hydrogen exchange of young rat skeletal muscle in hypertonic media.
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Evidence by calorimetry for an activation of sodium-hydrogen exchange of young rat skeletal muscle in hypertonic media.

机译:通过量热法证明高渗介质中年轻大鼠骨骼肌钠氢交换的激活。

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摘要

1. The rate of energy dissipation associated with Na(+)-H+ exchange in isolated, superfused soleus muscles from young rats was measured with an isothermal microcalorimeter during quasi-stationary states of oxidative metabolism. 2. Under normal physiological conditions, amiloride, an inhibitor of the Na(+)-H+ exchange across plasma membranes, had no measurable effect on the specific rate of muscle heat production (E); the ouabain-suppressible part of E was identical whether amiloride was absent or present. 3. E was increased under hyperosmotic conditions and the difference with respect to control (excess E) was proportional to the degree of hyperosmolarity of the superfusate. It was 48% of basal E during a +100 mosM stress (with no change of extracellular Na+ concentration, Na+o). Inhibition of Ca2+ release into the sarcoplasm with sodium dantrolene (10(-5) M) or tetracaine (5 x 10(-5) M) suppressed a substantial part (65 and 53%, respectively) of the steady-state excess E (1.2 mW (g wet weight)-1) induced by the +100 mosM stress. Practically 100% of excess E was suppressed in the nominal absence of extracellular sodium (Na+o = 0, Li+ substitution) or under 15 mM-Na+o, and excess E was enhanced when Na+o was increased (hyperosomolarity by addition of Na2SO4 instead of sucrose). 4. Under hyperosmotic conditions, amiloride at the 5 x 10(-7) M concentration had no effect on excess E whereas at 10(-4) M it induced a significant decrease of excess E. The absolute effect of 10(-4) M-amiloride was -0.34 mW (g wet weight)-1 (equal to 28% of the excess E due to a +100 mosM-sucrose stress and to 14% of the excess E due to a +100 mosM-Na2SO4 stress). It was left unaltered in the presence of dantrolene and was independent of the way the +100 mosM stress was obtained (i.e. 100 mM-sucrose or 50 mM-Na2SO4). It was suppressed at Na+o = 0-15 mM and could be mimicked by guanochlor, another potent inhibitor of Na(+)-H+ exchange. In the presence of 10(-4) M-amiloride, the ouabain-suppressible E was significantly reduced. In the presence of ouabain, amiloride had no effect. 5. Muscle tissue space available to [3H]inulin was measured in parallel experiments. It was 23.3% under control conditions and 30.6% after a 2 h exposure of the muscle to a +100 mosM-Na2SO4 stress.(ABSTRACT TRUNCATED AT 400 WORDS)
机译:1.用等温微量热仪在氧化代谢的准稳态期间测量与年轻大鼠离体的,融合的比目鱼肌中Na(+)-H +交换相关的能量耗散率。 2.在正常生理条件下,阿米洛利(一种跨质膜的Na(+)-H +交换抑制剂)对肌肉生热的比速率没有可测量的影响(E);无论是否存在阿米洛利,E的哇巴因可抑制部分是相同的。 3.在高渗条件下,E增加,相对于对照的差异(过量E)与超融合液的高渗程度成正比。在+100 mosM压力下(无细胞外Na +浓度,Na + o改变)为基础E的48%。用丹特罗钠(10(-5)M)或丁卡因(5 x 10(-5)M)抑制Ca2 +释放进入肌浆可抑制稳态过量E的很大一部分(分别为65%和53%)( +100 mosM应力引起1.2 mW(克湿重)-1)。在名义上不存在细胞外钠(Na + o = 0,Li +取代)或在15 mM-Na + o以下的情况下,几乎100%的过量E被抑制,当Na + o增加时,过量的E会增强(通过添加亚硫酸氢钾Na2SO4代替蔗糖)。 4.在高渗条件下,浓度为5 x 10(-7)M的阿米洛利对过量E没有影响,而在10(-4)M时,阿米洛利引起过量E明显降低。绝对值10(-4) M-阿米洛利为-0.34 mW(g湿重)-1(由于+100 mosM-蔗糖应力所致等于过量E的28%,由于+100 mosM-Na2SO4应力所致等于过量E的14%) 。在丹特罗的存在下保持不变,并且与获得+100 mosM应力的方式(即100 mM蔗糖或50 mM-Na2SO4)无关。它在Na + o = 0-15 mM时被抑制,可以被另一种有效的Na(+)-H +交换抑制剂胍氯仿。在10(-4)M-阿米洛利存在下,哇巴因可抑制的E显着降低。在哇巴因的存在下,阿米洛利没有作用。 5.在平行实验中测量[3 H]菊粉可用的肌肉组织空间。在对照条件下为23.3%,在肌肉暴露于+100 mosM-Na2SO4压力2小时后为30.6%(抽象截断为400个单词)

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