Arachidonic acid stimulates short-circuit current in the isolated toad urinary bladder.

The effects of the prostaglandin (PG) precursors 5,8,11,14-eicosatetraenoic acid (arachidonic acid) and 8,11,14-eicosatrienoic acid (dihomo-gamma-linolenic acid) on short-circuit current (SCC) were assessed in the isolated toad urinary bladder. Arachidonic acid added to the serosal bathing media increased SCC and immunoreactive PGE2 (iPGE2) synthesis in a dose-related manner. Pretreatment with eicosatetraynoic acid (50 micrometer), a prostaglandin synthetase inhibitor, completely blocked the arachidonic acid-induced increase in SCC and significantly reduced iPGE2 synthesis (P less than .025, n = 9). Eicosatrienoic acid (100 micrometer) was equieffective with arachidonic acid in increasing SCC and iPGE1 synthesis. Addition of arachidonic acid (100 micrometer) to the mucosal bathing media produced no significant increase in SCC and only increased iPGE2 synthesis from 0.03 +/- 0.01 pmol/min (n = 5) to 0.31 +/- 0.03 pmol/min, a level not different from the serosal basal rate of iPGE synthesis (0.21 +/- 0.16 pmol/min, n = 5). PGE1 (1 micrometer) added to the serosal media significantly increased SCC reaching a maximum increase of 157 +/- 43% (P less than .025, n = 6) by 30 min whereas addition to the mucosal media resulted in a delayed (60 min) and lesser maximum increase (59 +/- 19%, P less than .02, n = 6). It is concluded that prostaglandin precursors increase SCC and PGE synthesis in the isolated toad urinary bladder. However, the present data do not support PGE as the metabolite responsible for the increase in SCC.