Functional compartmentalization of oxidative and glycolytic metabolism in vascular smooth muscle.

The metabolism of vascular smooth muscle is characterized by an unusual component of aerobic glycolysis. Lactate production, even under fully oxygenated conditions, is of similar magnitude to the rate of oxygen consumption when compared on a molar basis. Although the underlying mechanisms are unknown, the ratio of glycolytic to oxidative metabolism has been suggested to be an index of vascular myopathy. Measurements of the rate of O2 consumption (JO2), lactate production (Jlac), and isometric force in porcine coronary arteries were made under conditions known to alter both active force (delta Po) and Na+-K+ transport. As previously reported, JO2 was strongly correlated with delta Po; Jlac, however, was correlated with conditions that alter Na+-K+ transport. Under conditions known to inhibit Na+-K+ transport (10(-5) M ouabain, absence of extracellular K+ or Na+), Jlac was inhibited even though delta Po and JO2 were increased. The coupling of Na+-K+ transport with aerobic glycolysis was not dependent on tonicity or the major anion species, nor was it an effect simply on tissue lactate permeability as indicated by studies of tissue lactate content. Metabolic measurements made at similar levels of delta Po indicate that Jlac is markedly inhibited by ouabain, whereas JO2 shows little effect. Thus the unusual aerobic glycolysis observed in vascular smooth muscle appears to be linked to Na+-K+ transport processes and not to some nonspecific metabolic deficiency. Experiments on both systemic and pulmonary arteries from rat, rabbit, dog, and pig indicate that these results are not limited solely to porcine coronary vessels.