Evidence that prostaglandin E2 stimulates chloride secretion in cultured A6 renal epithelial cells.
The effects of prostaglandin E2 (PGE2) on the transport of sodium and chloride were studied in cultured A6 renal epithelial cells. PGE2 on the basolateral but not the apical surface increased transmonolayer short-circuit current (Isc) and conductance. These changes could not be inhibited with amiloride or furosemide in the apical medium. Flux measurements showed that although Isc and net flux of sodium were equal in unstimulated cells, after addition of PGE2 the current increased with no corresponding changes in bidirectional or net flux of sodium. Immersing the cells in sodium-free or chloride-free media inhibited the effects of PGE2. Measurements of the simultaneous fluxes of sodium and chloride showed that after PGE2 was added there was a net flux of chloride from the basal to the apical side (secretion) that was equal to the change in Isc. The effects of PGE2 were inhibited by furosemide in the basal medium. We conclude that PGE2 stimulates a process of chloride secretion in A6 cells.
Keeler
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R
Wong
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D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001001:Anura; D002478:Cells, Cultured; D002712:Chlorides / Q000378:metabolism*; D015232:Dinoprostone; D004847:Epithelial Cells; D004848:Epithelium / Q000378:metabolism; D005665:Furosemide / Q000494:pharmacology; D007668:Kidney / Q000166:cytology / Q000378:metabolism*; D011458:Prostaglandins E / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism; D013268:Stimulation, Chemical
D002712:Chlorides; D011458:Prostaglandins E; D000584:Amiloride; D005665:Furosemide; D012964:Sodium; D015232:Dinoprostone