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Creatinine Transport by Basolateral Organic Cation Transporter hOCT2 in the Human Kidney
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Creatinine Transport by Basolateral Organic Cation Transporter hOCT2 in the Human Kidney
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Journal Article
Creatinine Transport by Basolateral Organic Cation Transporter hOCT2 in the Human Kidney
2004
Overview
Creatinine is excreted into urine by tubular secretion in addition to glomerular filtration. The purpose of this study was to clarify molecular mechanisms underlying the tubular secretion of creatinine in the human kidney.
Transport of [14C]creatinine by human organic ion transporters (SLC22A) was assessed by HEK293 cells expressing hOCT1, hOCT2, hOCT2-A, hOAT1, and hOAT3.
Among the organic ion transporters examined, only hOCT2 stimulated creatinine uptake when expressed in HEK293 cells. Creatinine uptake by hOCT2 was dependent on the membrane potential. The Michaelis constant (Km) for creatinine transport by hOCT2 was 4.0 mM, suggesting low affinity. Various cationic drugs including cimetidine and trimethoprim, but not anionic drugs, markedly inhibited creatinine uptake by hOCT2.
These results suggest that hOCT2, but not hOCT1, is responsible for the basolateral membrane transport of creatinine in the human kidney.
Publisher
Springer Nature B.V
Subject
1-Methyl-4-phenylpyridinium - pharmacology
/ Creatinine - antagonists & inhibitors
/ Dose-Response Relationship, Drug
/ Humans
/ Japan
/ Kidney Tubules - drug effects
/ Membrane Potentials - drug effects
/ Membrane Potentials - physiology
/ Organic Cation Transport Proteins - drug effects
/ Organic Cation Transport Proteins - genetics
/ Organic Cation Transport Proteins - metabolism
/ Organic Cation Transporter 1 - drug effects
/ Organic Cation Transporter 1 - genetics
/ Organic Cation Transporter 1 - metabolism
/ Organic Cation Transporter 2
/ Proteins
/ Tritium
/ Urine
