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Am J Physiol Renal Physiol (November 12, 2002). doi:10.1152/ajprenal.00290.2002
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Articles in PresS, published online ahead of print November 12, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00290.2002
Submitted on August 12, 2002
Accepted on November 5, 2002

Transport of cimetidine by flounder and human renal organic anion transporter 1

Birgitta C. Burckhardt1*, Stefan Brai1, Sonke Wallis1, Wolfgang Krick1, Natascha A. Wolff1, and Gerhard Burckhardt1

1 Abteilung Vegetative Physiologie und Pathophysiologie, Zentrum Physiologie und Pathophysiologie, Goettingen, Germany

* To whom correspondence should be addressed. E-mail: bcburckhardt{at}veg-physiol.med.uni-goettingen.de.

The H2-receptor antagonist cimetidine is efficiently excreted by the kidneys. In vivo studies indicated an interaction of cimetidine not only with transporters for basolateral uptake of organic cations, but also with those involved in excretion of organic anions. We therefore tested cimetidine as a possible substrate of the organic anion transporters cloned from winter flounder (fROAT) and from human kidney (hOAT1). Uptake of [3H]cimetidine into fROAT-expressing Xenopus laevis oocytes exceeded uptake into control oocytes. At -60 mV clamp potential, 1 mM cimetidine induced an inward current, which was smaller than that elicited by 0.1 mM PAH. Cimetidine concentrations exceeding 0.1 mM decreased PAH-induced inward currents, indicating interaction with the same transporter. At pH 6.6, no current was seen with 0.1 mM cimetidine, whereas at pH 8.6, a current was readily detectable, suggesting preferential translocation of uncharged cimetidine by fROAT. Oocytes expressing hOAT1 also showed [3H]cimetidine uptake. These data reveal cimetidine as a substrate for fROAT/hOAT1 and suggest that organic anion transporters contribute to cimetidine excretion in proximal tubules.




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