AJP - Heart and Circulatory Physiology, Vol 266, Issue 6 2239-H2246, Copyright © 1994 by American Physiological Society
Rubidium entry into brain and cerebrospinal fluid during acute and chronic alterations in plasma potassium
W. Stummer, R. F. Keep and A. L. Betz
Department of Surgery, University of Michigan, Ann Arbor 48109.
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.
