Prostaglandin E2 transport in rabbit renal basolateral membrane vesicles.
We examined the mechanism of prostaglandin E2 transport in rabbit renal basolateral membrane vesicles which were predominantly oriented right-side-out. In the presence of an inwardly directed H+ gradient, the initial rate of uptake was markedly accelerated and the influx of prostaglandin E2 resulted in a transient accumulation (overshoot) above the equilibrium value. Both H+-independent and H+-stimulated prostaglandin E2 uptake were shown to be insensitive to valinomycin-induced K+ diffusion potentials. Intravesicular probenecid inhibited the pH gradient-stimulated uptake of prostaglandin E2 but did not affect the pH-stimulated uptake of thiocyanate and acetate which enter membranes via ionic and nonionic diffusion, respectively. Finally, the existence of a Na+ cotransport or of a K+ antiport pathway for prostaglandin E2 could not be demonstrated. Thus, these data demonstrate the presence of an electrically neutral H+-prostaglandin E2 cotransport or OH- -prostaglandin E2 antiport mechanism in the basolateral membrane of the rabbit proximal tubule.
D000085:Acetates / Q000378:metabolism; D019342:Acetic Acid; D000818:Animals; D001485:Basement Membrane / Q000378:metabolism; D001693:Biological Transport, Active; D004058:Diffusion; D015232:Dinoprostone; D007668:Kidney / Q000648:ultrastructure*; D011188:Potassium / Q000378:metabolism; D011458:Prostaglandins E / Q000378:metabolism*; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D013861:Thiocyanates / Q000378:metabolism; D014634:Valinomycin / Q000494:pharmacology
D000085:Acetates; D011458:Prostaglandins E; D013861:Thiocyanates; D014634:Valinomycin; D012964:Sodium; D015232:Dinoprostone; C031760:thiocyanate; D019342:Acetic Acid; D011188:Potassium