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.