Hypoxanthine Uptake by Isolated Brain Microvessels

Abstract

Brain is among the most active tissues in nucleotide and nucleic acid synthesis (1) but the role of the blood brain barrier in regulating the transport of purine and pyrimidine has not, so far, well defined. The existence of a presynaptic purinergic modulation of trasmitter release in the central nervous system (1) emphasize a possibly important role of purine transport at the blood-brain barrier. Previous reports (2) have demonstrated the existence, on the luminal side of the blood-brain barrier, of two saturable purine transport systems, one is specific for adenine and hypoxanthine transport and the other one accounts for nucleoside transport. Recently Betz (3) has shown in isolated brain microvessels the existence of xanthine oxidase activity, as well as the capability of the isolated vessels to take up hypoxanthine which is subsequently degraded to xanthine and uric acid or incorporated in other compounds by energy dependent processes. The aim of this report was to establish whether, as in other tissues, in isolated brain microvessels, which are an in vitro model of the blood brain barrier, hypoxanthine transport and metabolism is regulated by the levels of inorganic phosphate and/or phosphate esters.