The role of transport processes in the distribution and disposition of prostaglandins

Abstract

Currently available evidence shows that some cell membranes represent a barrier to passive diffusion of PGs. In contrast, an active transport of PGs was demonstrated across the wall of the rabbit vagina in vitro. Evidence has been obtained indicating that similar carrier-mediated PG transport processes in vivo mediate the uptake of PGs from the circulation into the lung and the removal of these autocoids from the brain and the eye, across the blood--brain and blood--aqueous barriers. It was shown that probenecid, a known inhibitor of PG transport, enhances the effect of PGE1 on the brain, and in general, it appears to alter the distribution and rate of excretion of PGs. The existence of such barriers to the free diffusion of PGs and the saturable, and possibly rate-limiting, transport of these autocoids across some other membranes must be taken into consideration in the design of experiments and in the interpretation of results. Furthermore, the importance of this consideration is emphasized by the observation that many nonsteroidal antiinflammatory agents and PG antagonists are effective inhibitors of PG transport (17,18); hence, they can be expected to affect the distribution and disposition of PGs.