Effect of PGI2 on transcellular transport of fluorescein dextran through an arterial endothelial monolayer.
The effects of prostacyclin (PGI2) and stable derivatives of PGI2, such as isocarbacyclin (PGI2 deriv. (A] and isocarbacyclin methyl ester (PGI2 deriv. (B)), on junctional transport of fluorescein dextran (FD) through cultured porcine arterial endothelial cells were investigated. These PGI2S inhibited the transcellular transport dose-dependently. After the elimination of PGI2, its inhibitory effect persisted for at least 1 hr. A good correlation was found between increase of cAMP and the potency of inhibition. Increase of cAMP after PGI2 treatment seemed to be involved in the inhibition of FD transport.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism; D003911:Dextrans / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D011464:Epoprostenol / Q000494:pharmacology* / Q000031:analogs & derivatives; D005452:Fluoresceins / Q000378:metabolism*; D007365:Intercellular Junctions / Q000378:metabolism; D013552:Swine
D003911:Dextrans; D005452:Fluoresceins; C052526:fluorescein-dextran; C052840:TEI 9090; C041946:9-O-methanoprostaglandin I; D011464:Epoprostenol; D000242:Cyclic AMP; D015056:1-Methyl-3-isobutylxanthine