Leukotriene C4 transport by the choroid plexus in vitro

Nanomolar concentrations of peptidoleukotrienes evoke sustained cerebral edema and arterial constriction. Peptidoleukotrienes are thus considered to play an important role in eliciting cerebral edema after cerebral ischemia and vasospasm after subarachnoid hemorrhage. It was hypothesized that the choroid plexus, the locus of the blood-cerebrospinal fluid barrier, might minimize the vasoactivity of locally generated or systemically derived leukotrienes by transporting leukotrienes from cerebrospinal fluid into the blood. Consistent with this hypothesis, leukotriene C4 in vitro was transported into and released from isolated rabbit choroid plexus by a system that was specific, energy-dependent, probenecid-sensitive, and depressed by cold temperatures. The accumulation of leukotriene C4 in the choroid plexus was not dependent on tissue binding or metabolism of leukotriene C4.