Abstract
1. The specific contributions of aerobic glycolysis and oxidative metabolism to Na+ pump activity were quantitated in porcine carotid arteries under aerobic conditions. 2. Active reaccumulation of potassium by potassium‐depleted tissues could be supported by oxidative metabolism alone, anaerobic metabolism in the presence of glucose, or a combination of oxidative metabolism and aerobic glycolysis, but not under anaerobic conditions in the absence of glucose. 3. Increasing levels of potassium added to potassium‐depleted arteries under aerobic conditions resulted first in stimulation of aerobic lactate release which saturated at 0.028‐0.036 mumol min‐1 g‐1, which was then followed by a stimulation of oxidative metabolism. This behaviour is opposite to the classic Pasteur effect. 4. The dependence of potassium uptake and lactate release on the concentration of potassium added to potassium‐depleted arteries ('potassium re‐entry concentration') under aerobic conditions were qualitatively similar. The K0.5 (concentration at which the velocity is half‐maximally activated) and Vmax (the maximum velocity) for lactate release were 1.2 +/‐ 0.3 mM and 0.037 mumol min‐1 g‐1, respectively; those for K+ uptake were 4.3 +/‐ 0.4 mM and 0.399 mumol min‐1 g‐1. 5. The stoichiometric ratio between potassium uptake and ATP as calculated from lactate release approximated theoretical values of 2:1 (assuming 1 ATP per lactate) when potassium re‐entry concentrations were less than 2 mM; higher concentrations of potassium produced ratios up to 9:1. 6. Physiological pump rates, as determined by potassium efflux studies, corresponded to potassium re‐entry concentrations of less than or equal to 2 mM, the same potassium re‐entry concentrations where the stoichiometry between potassium transport and aerobic glycolysis approximated the theoretical ratio of 2:1. Increases in oxidative metabolism were not detected in this range, but were detected at potassium re‐entry concentrations of greater than or equal to 4 mM. 7. It was concluded that at physiological Na+ pump rates, aerobic glycolytic metabolism supported the N+,K(+)‐ATPase; at higher pump rates, oxidative metabolism was required for pump support as well.