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Vol. 301, Issue 1, 293-298, April 2002
Department of Pharmacology and Toxicology, Kyorin University School
of Medicine, Tokyo, Japan (M.T., S.N., A.E., H.E.); and Division of
Nephrology and Hypertension, Department of Internal Medicine, Jikeikai
University School of Medicine, Tokyo, Japan (H.K., K.I.)
Prostaglandin E2 (PGE2) and prostaglandin
F2
(PGF2) have been used for the
induction of labor and the termination of pregnancy. Renal excretion is
shown to be an important pathway for the elimination of
PGE2 and PGF2. The purpose of this study was
to elucidate the molecular mechanism of renal PGE2 and PGF2 transport using cells stably expressing human
organic anion transporter (hOAT) 1, hOAT2, hOAT3, and hOAT4, and human organic cation transporter (hOCT) 1 and hOCT2. A time- and
dose-dependent increase in PGE2 and PGF2
uptake was observed in cells expressing hOAT1, hOAT2, hOAT3, hOAT4,
hOCT1, and hOCT2. The Km values of PGE2 uptake by hOAT1, hOAT2, hOAT3, hOAT4, hOCT1, and hOCT2
were 970, 713, 345, 154, 657, and 28.9 nM, respectively, whereas those of PGF2 uptake by hOAT1, hOAT3, hOAT4, hOCT1, and hOCT2
were 575, 1092, 692, 477, and 334 nM, respectively. PGE2
and PGF2 significantly inhibited organic anion uptake by
hOATs and organic cation uptake by hOCTs. In conclusion, considering
the localization of these transporters, the results suggest that
PGE2 and PGF2 transport in the basolateral
membrane of the proximal tubule is mediated by multiple pathways
including hOAT1, hOAT2, hOAT3, and hOCT2, whereas that in the apical
side is mediated by hOAT4.
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