Abstract
Pathways for transport of ethanolamine by human placental epithelia were investigated by measurement of [3H]ethanolamine uptake in brush-border membrane vesicles isolated by divalent cation precipitation. The presence of a conductive uptake pathway for ethanolamine was suggested by the marked stimulation of ethanolamine uptake to levels exceeding equilibrium induced by an inside-negative potassium diffusion potential. Evidence to suggest conductive ethanolamine uptake resulted from a mediated transport process included 1) the concentration-dependent inhibition by choline; 2) trans-stimulation of choline and ethanolamine uptake by ethanolamine; and 3) substrate-specific inhibition by chemically related analogs. Transport of both choline and ethanolamine by a common facilitated diffusion mechanism is suggested by 1) trans-stimulation of choline uptake by ethanolamine; 2) mutual inhibition of conductive choline and ethanolamine uptake by ethanolamine and choline; 3) the effect of ethanolamine on the kinetics of conductive choline uptake; and 4) the rank order inhibition of choline and ethanolamine uptake by the same panel of chemical analogs. The present study identifies the presence of a facilitated diffusion mechanism as a brush-border membrane transport pathway for choline and ethanolamine accumulation by human placenta.
Footnotes
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This work was supported by National Institutes of Health Grant HD29940 and the American Heart Association, New York State Affiliate.
- Abbreviations:
- FCCP
- carbonylcyanidep-trifluoromethoxyphenylhydrazone
- SQI
- N1N-bis-(2-methyl-5,6-diethoxy-9-quinolyl)-diaza[15]-crown-5
- MES
- 4-morpholineethanesulfonic acid
- Received March 6, 2001.
- Accepted April 23, 2001.
- The American Society for Pharmacology and Experimental Therapeutics
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