Tubular prostaglandin E2 production and its role in urinary hypotonicity after release of ureteral occlusion in the rat.

Abstract

1. In order to explore the involvement of endogenous prostaglandin E2 (PGE2) in the urine concentration defect after ureteral occlusion, PGE2 production by isolated collecting ducts in vitro and effects of indomethacin on urine osmolality in vivo were examined. 2. Twenty-four hours ureter obstruction caused increased PGE2 production by the medullary collecting ducts, which was maintained at a high level on the day after release of obstruction (0.8 +/- 0.2 pg/mm normal, 8.1 +/- 0.9 pg/mm 24 h obstruction, and 6.6 +/- 1.0 pg/mm post-obstruction, mean +/- SEM). An enhanced PGE2 production was also observed for papillary collecting duct on the day after release of 24 h ureteral occlusion (3.9 +/- 0.5 pg/mm normal and 7.7 +/- 1.2 pg/mm post-obstruction). 3. Administration of indomethacin to the unilateral post-obstructive rats slightly raised the urine osmolality of the post-obstructed kidney (from 339 +/- 17 to 390 +/- 22 mosmol/kg H2O), while it had a greater effect on the contralateral intact kidney (from 1569 +/- 138 to 2567 +/- 198 mosmol/kg H2O). 4. Our data may indicate that the urine concentration defect after 24 h ureteral occlusion is ascribable mainly to a mechanism other than increased endogenous PGE2.