Abstract

Partial outlet obstruction of the urinary bladder has been demonstrated to induce specific dysfunctions in cellular and sub-cellular membrane structures within the bladder’s smooth muscle and mucosal compartments. Recent studies have linked these membrane dysfunctions to alterations in phospholipid metabolism leading to mobilization of free arachidonic acid, the precursor for synthesis of prostaglandins (PG). The purpose of this study was to determine if partial outlet obstruction of the urinary bladder induces changes in the capacity of bladder smooth muscle and mucosa to generate PG. PG were isolated from control and partially obstructed urinary bladder smooth muscle and mucosa of male New Zealand White (NZW) rabbits. PG concentrations (PGE 2, PGF 2α, and PGI 2, as its stable metabolite 6-keto-PGF 1α) were determined after 30 minute incubations using enzyme-linked immunoassay (ELISA) kits. In both control and obstructed rabbit urinary bladders, PG generation was significantly higher in isolated mucosa than muscle tissues. A significantly higher concentration of PGF 2α, and 6-keto-PGF 1α was measured in obstructed muscle tissue relative to controls. The concentration of 6-keto-PGF 1α was also significantly higher than the concentrations measured for PGE 2 and PGF 2α in both control and obstructed smooth muscle samples. The generation of PGE 2 was significantly higher in rabbit urinary bladder mucosa than either PGF 2α or 6-keto-PGF 1α in both control and obstructed samples. The capacity of obstructed mucosal tissue to generate 6-keto-PGF 1α was significantly higher than control tissue, while no significant differences in PGE or PGF 2α generation were noted. These data suggest obstruction of the urinary bladder induce specific elevations in PG in both smooth muscle and mucosal tissues.

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