Abstract
Arginine vasopressin (AVP) changes the kinetic parameters of the blood-brain barrier (BBB) transport of large neutral amino acids (LNAA). The effect is believed to result from the occupation of V1 receptors at the luminal surface of brain endothelial cells which in turn induces allosteric changes in the LNAA transporter, the L system. These changes result in a diminished unidirectional influx of all LNAA to the brain. In addition, circulating AVP is also known to reduce amino acid levels in brain extracellular fluid (ECF) as measured in cerebrospinal fluid (CSF). In the present paper we discuss the extent to which changes in BBB transport might account for the observed changes in the CSF concentrations of LNAA. A comparative analysis of our data suggests that the reduced influx of LNAA across the BBB cannot fully explain the observed reduction in CSF levels. Thus other effects induced by the peptide such as changes in the production rate of ECF and CSF or a stimulation of amino acid uptake by brain cells might be involved.
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