Sodium transport in capillaries isolated from rat brain.

Brain capillary endothelial cells form a blood-brain barrier (BBB) that appears to play a role in fluid and ion homeostasis in brain. One important transport system that may be involved in this regulatory function is the Na+, K+-ATPase that was previously demonstrated to be present in isolated brain capillaries. The goal of the present study was to identify additional Na+ transport systems in brain capillaries that might contribute to BBB function. Microvessels were isolated from rat brains and 22Na+ uptake by and efflux from the cells were studied. Total 22Na+ uptake was increased and the rate of 22Na+ efflux was decreased by ouabain, confirming the presence of Na+, K+-ATPase in capillary cells. After inhibition of Na+, K+-ATPase activity, another saturable Na+ transport mechanism became apparent. Capillary uptake of 22Na+ was stimulated by an elevated concentration of Na+ or H+ inside the cells and inhibited by extracellular Na+, H+, Li+, and NH4+. Amiloride inhibited 22Na+ uptake with a Ki between 10(-5) and 10(-6) M but there was no effect of 1 mM furosemide on 22Na+ uptake by the isolated microvessels. These results indicate the presence in brain capillaries of a transport system capable of mediating Na+/Na+ and Na+/H+ exchange. As a similar transport system does not appear to be present on the luminal membrane of the brain capillary endothelial cell, it is proposed that Na+/H+ exchange occurs primarily across the antiluminal membrane.