Sahlin K, Gorski J, Edström L
Department of Clinical Physiology, Huddinge Hospital, Sweden.
Am J Physiol. 1990 Sep;259(3 Pt 1):C409-12. doi: 10.1152/ajpcell.1990.259.3.C409.
Deamination of AMP to inosine monophosphate (IMP) and NH3 is thought to be regulated by the observed increases in ADP, AMP, and H+. We have examined this hypothesis by comparing the rate of IMP accumulation in contracting and noncontracting rat skeletal muscle. The rate of IMP formation was high during ischemic contraction, and consistent with previous studies, formation of IMP was associated with high levels of muscle lactate, depletion of phosphocreatine (PCr), and increased levels of ADP and AMP. When the contraction period was followed by 5-min anoxic recovery, the metabolic changes were maintained, but no further IMP or lactate was formed. During long-term (2-4 h) anoxia, the rate of IMP formation was less than 4% of that during contraction, despite similar changes in PCr, lactate, ADP, and AMP. It is concluded that the observed changes in the intracellular chemical environment are not sufficient to explain the high rate of IMP formation during contraction but that a combination of metabolic stress and a high ATP turnover rate is required. It is suggested that a high ATP turnover rate during conditions of metabolic stress results in transient increases in ADP and AMP at the site of ATP hydrolysis and that these activate AMP deaminase and glycolysis. An alternative hypothesis is that these processes are regulated by the increase in cytosolic Ca2+ in a contracting muscle.
AMP脱氨生成肌苷一磷酸（IMP）和NH3被认为受观察到的ADP、AMP和H+增加的调节。我们通过比较收缩和不收缩的大鼠骨骼肌中IMP积累的速率来检验这一假设。在缺血收缩期间，IMP形成的速率很高，并且与先前的研究一致，IMP的形成与肌肉乳酸水平升高、磷酸肌酸（PCr）耗竭以及ADP和AMP水平升高有关。当收缩期之后进行5分钟的缺氧恢复时，代谢变化得以维持，但没有进一步形成IMP或乳酸。在长期（2 - 4小时）缺氧期间，尽管PCr、乳酸、ADP和AMP有类似变化，但IMP形成的速率不到收缩期间的4%。结论是，观察到的细胞内化学环境变化不足以解释收缩期间IMP形成的高速率，而是需要代谢应激和高ATP周转率的结合。有人提出，在代谢应激条件下高ATP周转率会导致ATP水解部位的ADP和AMP短暂增加，并且这些会激活AMP脱氨酶和糖酵解。另一种假设是这些过程受收缩肌肉中细胞溶质Ca2+增加的调节。
