Chloride secretion stimulated by prostaglandin E1 and by forskolin in a canine renal epithelial cell line.

1. The actions of prostaglandins upon ion transport in a renal-derived cultured epithelium (MDCK) have been investigated. 2. Prostaglandin E1 (PGE1) stimulates an inwards short-circuit current (SCC) in voltage-clamped epithelial layers mounted in Ussing chambers. Measurements of transepithelial Cl- fluxes, cation and anion replacement of the bathing media and the use of the Cl- channel blocker 3-nitro-2(3-phenylpropylamino)-benzoic acid (NPPB) are consistent with the PGE1-stimulated inward SCC resulting predominantly from basal to apical Cl- secretion. 3. The response of MDCK epithelia is relatively specific for prostaglandins of the E series. PGE1 is most effective when applied to the basal bathing solutions, though near-maximal stimulation of SCC was possible with 1 microM-PGE1 added to the apical bathing solution. 4. Forskolin addition (10 microM) stimulates an inwards SCC in MDCK epithelia which displays similar characteristics and is of a similar magnitude to that observed with PGE1. In the presence of isobutylmethylzanthine, PGE1 and forskolin are capable of elevating intracellular cyclic AMP accumulation, suggesting that stimulation of inward SCC is mediated via a cyclic AMP-dependent mechanism.