Glycolysis and oxidative phosphorylation during activation of the sodium pump in the taenia from guinea-pig caecum.
1. In the taenia from the guinea-pig caecum, the relative contribution of glycolysis and oxidative phosphorylation to activation of the Na pump was estimated by measuring changes in the rate of O2 consumption (QO2) and lactate production (Q1act). The Na pump was activated by K readmission following prior treatment with K-free solution. The QO2 and Q1act were both increased significantly by K readmission 60 min after exposure to K-free solution. These changes and the reaccumulation of tissue K were abolished by ouabain (10 microM). Spontaneous mechanical activity ceased in K-free solution and the K-induced increase in QO2 and Q1act was produced before the mechanical activity was restarted. 2. Similar changes were obtained when ouabain (10 microM) was removed after 60 min treatment. It was estimated from the changes in QO2 and Q1act that the oxidative and glycolytic metabolism each supplied about 50% of the total ATP demand for pump activation. 3. In Ca-free solution, the increase in QO2 caused by K readmission was transient and QO2 returned to the previous value in K-free solution in 10-20 min. However, the increase in QO2 was maintained in the absence of glucose. When glucose was replaced with beta-hydroxybutyrate (beta-HB, 11.8 mM), which is metabolized only through oxidative phosphorylation, K readmission also produced a sustained increase in QO2. 4. In glycogen-depleted preparations, K readmission produced little or no increase in QO2 in the absence of substrate or in the presence of glucose. On the other hand, in the presence of beta-HB (11.8 mM), a typical increase in QO2 (about 0.1 mumol min-1 g-1) was observed in response to K readmission. Lactate production was negligible in the absence of substrate or in the presence of beta-HB, but it was significantly increased after K readmission in the presence of glucose. The increase in tissue K content following K readmission was the same in the presence of glucose or beta-HB. 5. In the glycogen-depleted preparations the increase in QO2 caused by beta-HB was dependent on the presence of both Na and K in the medium, and sensitive to ouabain. Furthermore, this response was reversibly suppressed by glucose.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D002432:Cecum / Q000502:physiology; D005260:Female; D005947:Glucose / Q000494:pharmacology; D006019:Glycolysis / Q000187:drug effects*; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects*; D007537:Isometric Contraction; D008297:Male; D009130:Muscle, Smooth / Q000502:physiology*; D010042:Ouabain / Q000494:pharmacology; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism* / Q000494:pharmacology
D007473:Ion Channels; D010042:Ouabain; D012964:Sodium; D005947:Glucose; D011188:Potassium