Interleukin-1 regulation of prostaglandin E2 synthesis by the papillary collecting duct.

Interleukin-1 (IL-1) has been demonstrated to cause a natriuresis and diuresis in experimental animals. This effect is associated with an increase in prostaglandin E2 (PGE2) excretion and is prevented by pretreatment with cyclooxygenase inhibitors. Micropuncture studies have shown IL-1 inhibition of sodium reabsorption by the rat papillary collecting duct (PCD), a nephron segment capable of abundant PGE2 synthesis. The current study examined the effect of IL-1 on PGE2 synthesis by cultured PCD cells and the mechanism by which such regulation occurs. IL-1 markedly increased PCD cell PGE2 synthesis within 15 minutes of exposure in a dose-dependent manner. Preincubation with saturating concentrations of arachidonic acid abolished IL-1 stimulation of PGE2 synthesis. PCD cells labeled with tritiated arachidonic acid released significantly more arachidonic acid within 5 minutes of exposure to IL-1 as compared to control cells. These data demonstrate that IL-1 directly stimulates PGE2 synthesis by PCD cells and that this effect occurs by enhancement of arachidonic acid release.