EFFECTS OF POTASSIUM AND LITHIUM ON SODIUM TRANSPORT FROM BLOOD TO CEREBROSPINAL FLUID

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Abstract
Abstract— The relationship between isotopic sodium entry into cerebrospinal fluid (CSF) from blood and cisternal potassium concentration was studied using ventriculo‐cisternal perfusion in the rabbit. The entry of sodium into CSF was separated into 2 components. The fast component was significantly correlated with cisternal potassium concentration during perfusions with a potassium‐free artificial CSF. ATPase activity in the homogenised choroid plexus was shown to be sensitive to potassium over a range of concentrations similar to that in the perfusion studies. The results are interpreted as showing a potassium‐sensitive entry of 24Na across the choroid plexus due to a sodium‐pump situated in the apical membrane of the choroid plexus. The effects of low concentrations of lithium (0.6–1.2 mm) on 24Na entry into CSF and brain and on CSF secretion were studied. When applied via the ventricles lithium caused a 30–39% stimulation of the fast component of sodium entry and a 28% stimulation of CSF secretion. When given via the blood lithium inhibited the fast component of sodium entry and CSF secretion by 43% and 40% respectively. No effects of lithium were found on the slow component of sodium entry into CSF or sodium entry into brain. The results suggest that lithium at low (0.6–1.2 mM) concentrations can stimulate the choroid plexus sodium‐pump at the potassium‐sensitive side and inhibit it at the sodium‐sensitive side.