Interference by prostaglandin E2 with the phosphaturic effects of nonhormonal agents.

The purpose of the present study was to evaluate the ability of prostaglandin (PG) E2 to alter phosphate excretory patterns induced by the nonhormonally mediated phosphaturic maneuvers, bicarbonate loading (BIC), volume expansion (VE) and acetazolamide administration (Az). Acute clearance studies were performed in chronically thyroparathyroid-ectomized dogs. The dosage of PGE2 utilized was free of excretory or hemodynamic effects. After BIC, percentage of phosphate excretion (%EP) increased from 4.8 to 14.0%, (P less than .05). In contrast, BIC preceded by PGE2 infusion produced no phosphaturia. Additionally, PGE2 blunted the increases in Na and HCO3 excretion associated with BIC. VE (5-6% b.wt.) increased %EP from 6.0 to 14.2%, (P less than .01). However, VE after PGE2 treatment did not result in a phosphaturia. Az increased %EP from 4.7 to 28.5%, (P less than .02). When PGE2 was infused before Az, %EP rose from 1.9 to 7.1%, (P less than .02) in response to Az. However, the increment in %EP over base line was reduced from 23.8 to 3.6% by PGE2 pretreatment (P less than .005). PGE2 did not alter the effects of VE or Az on sodium or bicarbonate excretion. Thus, PGE2 blunts or abolishes the phosphaturic effect of each of these maneuvers independent of its action on sodium or bicarbonate transport. We conclude that PGs have a specific action on phosphate transport events induced by certain nonhormonal factors, revealing a hitherto unappreciated role for these agents in modulating tubular reabsorptive processes.