Rubidium entry into brain and cerebrospinal fluid during acute and chronic alterations in plasma potassium

To elucidate whether K+ uptake across the blood-brain barrier (BBB) or blood-cerebrospinal fluid (CSF) barrier is subject to acute or chronic regulation, rats were rendered acutely or chronically hyper- or hypokalemic (range: 2.8-7.2 mM). Measurements were made of the permeability-surface (PS) products of 86Rb+, a marker for K+, and alpha-[3H]aminoisobutyric acid (AIB), a passive permeability marker, and of CSF K+ concentration ([K+]CSF). [K+]CSF decreased by 8% in chronic hypokalemia P < 0.01), but otherwise remained unchanged. The AIB PS products were unaltered in any group, excluding a change in passive permeability. The Rb PS product, however, increased by 31% for brain tissue (P < 0.01) and by 46% for CSF (P < 0.05) during acute hypokalemia, but was unchanged during acute hyperkalemia. During chronic hypokalemia the Rb PS product increased by 40% for brain (P < 0.01) and 55% for CSF (P < 0.01) and decreased during chronic hyperkalemia by 37% for brain (P < 0.01) and 49% (P < 0.01) for CSF. Unidirectional K+ fluxes were calculated, revealing greater regulation of K+ influx into both brain tissue and CSF during chronic compared with acute changes of plasma K+ concentration ([K+]pl). Our results suggest that K+ transport is saturable at both the BBB and the blood-CSF barriers under normal conditions and that both barriers adapt to chronic changes in [K+]pl by modifying specific, transcellular routes of K+ entry.