AJP - Renal Physiology, Vol 233, Issue 2 133-F137, Copyright © 1977 by American Physiological Society
Renal tubular transport of prostaglandins: inhibition by probenecid and indomethacin
B. R. Rennick
With use of the Sperber technique in chickens, labeled prostaglandin E2 and
F2alpha were infused and resulted in renal tubular excretion of the label
into the urine. A labeled metabolite, 12,14-dihydro,15-keto-PGF2alpha, was
infused exogenously and this label was also excreted by active tubular
transport. Tubular excretion of the label from PGE2, PGF2alpha, and
13,14-dihydro,15-keto-PGF2alpha was inhibited by probenecid, indomethacin,
and PAH. The PAH was 10 times weaker as an inhibitor than probenecid and
indomethacin. These results indicate that the prostaglandins are actively
transported across the renal tubule by the classic anionic transport system
which transports PAH. Since the transport of the prostaglandins is blocked
by nonsteroidal anti-inflammatory agents such as indomethacin, the
anti-inflammatory action of indomethacin may be produced not only by the
inhibition of prostaglandin synthesis but also by restriction of the
distribution of endogenous prostaglnadins. Thin-layer chromatography of an
ethyl acetate extract of urine collected during infusion of [3H]PGF2alpha
revealed three discrete radioactive peaks, one of which corresponded to
authentic PGF2alpha. This signified tubular excretion of PGF2alpha. One
metabolite in the ethyl acetate extract was found to be of renal origin.
