Interactions of vasopressin, prostaglandins, and cAMP in rat renal papillary collecting tubule cells in culture.

To evaluate the hypothesis that prostaglandins (PGs) inhibit vasopressin stimulation of adenylate cyclase in the collecting tubule, we have studied the interactions of vasopressin, PGs, and intracellular cAMP in rat renal papillary collecting tubule (RPCT) cells in cell culture. Inhibition of PGE2 synthesis with acetylsalicylic acid (ASA) did not potentiate arginine vasopressin (AVP)-stimulated intracellular cAMP. Augmentation of prostanoid synthesis with arachidonic acid or exogenous addition of PGE2 did not decrease AVP-stimulated cAMP in the RPCT cells. Arachidonic acid or PGE2, used alone, increased cAMP and ASA reduced cAMP, consistent with the presence of a PG-sensitive adenylate cyclase. Six-hour incubations of RPCT cells produced clear evidence of homologous desensitization of the PGE2 receptor, after exposure to either PGE2 or arachidonic acid, but not heterologous desensitization of the AVP receptor linked to cAMP synthesis. Preincubation of the RPCT cells with AVP or 1-desamino-8-D-arginine vasopressin (dDAVP) induced homologous desensitization of AVP- or dDAVP-stimulated cAMP. Three-day incubations with dDAVP or AVP apparently induced cyclooxygenase activity since PGE2 synthesis increased in response to arachidonic acid and recovery of cyclooxygenase activity after ASA was enhanced by dDAVP or AVP. In conclusion, our data on AVP-stimulated cAMP in cultured RPCT cells do not support the hypothesis that PGE2 inhibits AVP-dependent collecting tubule cAMP.