Relation of potassium transport to oxidative metabolism in isolated brain capillaries

Abstract

The uptake of K by a capillary suspension isolated from rat brain was studied with the radioactive analog 86Rb. Rb uptake was dependent on the presence of O2 and could be markedly inhibited with ouabain. The ouabain sensitive Rb uptake was measured at varying external concentrations of K. Uptake of K (as 86Rb) was half-maximal when the K concentration was 3.0 mM. This in vitro affinity of the transport carrier for K is similar to that found in previous in vivo studies of K efflux from brain to blood. The ouabain sensitive K pump may be located on the antiluminal plasma membrane of brain capillary endothelial cells and this pump contributes to the maintenance of a constant concentration (i.e., 3 mM) of K in brain interstitial fluid. Glucose and palmitate were tested as possible energy substrates for the support of active Rb uptake by isolated brain capillaries. The rate of Rb uptake increased 40% when 0.25 mM-palmitate was added to a capillary suspension containing 5 mM glucose. Stimulation of Rb uptake could be blocked by 1 mM-4-pentenoic acid, an inhibitor of fatty acid oxidation. The fraction of Rb uptake supported by glucose was not altered by 4-pentenoic acid. The rates of [U(uniformly labeled)-14C]glucose and [U-14C]palmitate oxidation to CO2 were measured in isolated brain capillaries and compared to their oxidation by brain slices and synaptosomes. Palmitate was the source of 28% of the 14CO2 produced by the capillaries but only 0.5% of the 14CO2 produced by the brain slices and synaptosomes. Brain capillaries are similar to renal tubules in their polar distribution of ouabain sensitive K transport carriers, dependence on oxidative metabolism for active ion transport and use of fatty acids as energy substrates. These features may underlie the vulnerability of brain capillaries in several metabolic diseases that cause brain edema.