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To investigate the relationship of renal prostaglandin E2 (PGE2) synthesis to medullary interstitial osmolality, rat renal papillary collecting tubule (RPCT) cells in culture were exposed to media with different osmolaties. PGE2 released into the media was measured by radioimmunoassay. Increasing osmolality with equiosmolar sodium chloride and urea from 300 to 900 mOsm slightly increased PGE2 synthesis, whereas further increase above 1200 mOsm markedly inhibited PGE2 synthesis in RPCT cells. Hyperosmolar media also inhibited calcium ionophore-stimulated PGE2 synthesis, but did not inhibit arachidonate-stimulated PGE2 synthesis. In contrast, decreasing osmolality from 1800 to 300 mOsm induced a prominent but transient increase in PGE2 synthesis. This increase was abolished by TMB-8, an intracellular calcium antagonist, and trifluoperazine, a calmodulin antagonist. Osmolar increments with sodium chloride or urea alone resulted in the similar inhibition of PGE2 synthesis by sodium chloride but not by urea. These results indicate that extracellular sodium chloride inhibits PGE2 synthesis in RPCT cells at the step of arachidonic acid release, possibly at phospholipases, in a calcium-dependent manner.

Effect of sodium chloride on prostaglandin E2 synthesis in rat renal papillary collecting tubule cells in culture.