Reversibility of mechanical and biochemical changes in smooth muscle due to anoxia and substrate depletion.

The effect of temporary glucose and oxygen deprivation on isometric tension as well as content of glycogen, creatine phosphate (CP), adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenylate pool (AP) were studied in potassium-contracted guinea pig isolated taenia coli. Under aerobic conditions glucose removal caused a decrease in tension, glycogen, CP, ATP, and energy charge; ADP and AMP increased, keeping the adenylate pool size unchanged. During rigor caused by additional anoxia, there was an increase in tension associated with further decrease in ATP and marked reduction of adenylate pool. Restoration of oxygen supply caused only a small increase in ATP that, though sufficient for abolishing rigor, was insufficient to support potassium contraction. Restoration of both glucose and oxygen did not restore tension even though ATP stores were increased further. Elevation of extracellular calcium caused partial restoration of tension, suggesting that the defect was in calcium metabolism rather than energy metabolism. During recovery AP remained low, possibly due to deamination of AMP. Anoxia in the presence of glucose reduced ATP to a concentration similar to that due to aerobic glucose deprivation but tension decreased much less. This result is consistent with different degrees of ATP depletion in various functional (Ca pump vs. contractile mechanism) compartments.