Abstract

To determine the influence of prostaglandins on cAMP metabolism in renal papillary collecting tubule (RPCT) cells, intracellular cAMP levels were measured after incubating cells with prostaglandins (PGs) alone or in combination with arginine vasopressin (AVP). PGE 1, PGE 2 and PGI 2, but not PGD 2 or PGF 2α, increased intracellular cAMP concentrations. At maximal concentrations (10 −5 M tthe effects of PGE 2 plus PGI 2 (or PGE 1), but not of PGI 2 plus PGE 1, were additive suggesting that at least two different PG receptors may be present in RPCT cell populations. Bradykinin treatment of RPCT cells caused an accumulation of intracellular cAMP which was blocked by aspirin and was quantitatively similar to that observed with 10 −5 M PGE 2. PGs, when tested at concentrations (e.g. 10 −9 M ) which had no independent effect on intracellular cAMP levels, did not inhibit the AVP-induced accumulation of intracellular cAMP in RPCT cells. These results indicate that PGs do not block AVP-induced accumulation of intracellular cAMP in RPCT cells at concentrations of PGs which have been shown to inhibit the hydroosmatic effect of AVP on perfused collecting tubule segments. However, at higher concentrations of PGs (e.g. 10 −5 M ), the effects of AVP plus PGE 1, PGE 2, PGI 2 or bradykinin on intracellular cAMP levels were not additive. Thus, under certain conditions, there is an interaction between PGs and AVP at the level of cAMP metabolism in RPCT cells.

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