ARACHIDONIC-ACID STIMULATES SHORT-CIRCUIT CURRENT IN THE ISOLATED TOAD URINARY-BLADDER

  • 1 January 1980
    • journal article
    • research article
    • Vol. 213  (3) , 462-467
Abstract
The effects of the prostaglandin (PG) precursors 5,8,11,14-eicosatetraenoic acid (arachidonic acid [AA]) and 8,11,14-eicosatrienoic acid (dihomo-.gamma.-linolenic acid) on short-circuit current (SCC) were assessed in the isolated toad urinary bladder. AA added to the serosal bathing media increased SCC and immunoreactive (i2) PGE2 synthesis in a dose-related manner. Pretreatment with eicosatetraynoic acid (50 .mu.M), a PG synthetase inhibitor, completely blocked the AA-induced increase in SCC and significantly reduced iPGE2 synthesis (P < 0.025, no. = 9). Eicosatrienoic acid (100 .mu.M) was equieffective with AA in increasing SCC and iPGE1 synthesis. Addition of AA (100 .mu.M) to the mucosal bathing media produced no significant increase in SCC and only increased iPGE2 synthesis from 0.03 .+-. 0.01 pmol/min (no. = 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, no. = 5). PGE1 (1 .mu.M) added to the serosal media significantly increased SCC, reaching a maximum increase of 157 .+-. 43% (P < 0.025, no. 6) by 30 min but addition to the mucosal media caused a delayed (60 min) and lesser maximum increase (59 .+-. 19%, P < 0.02, no. = 6). Apparently PG precursors increase SCC and PGE synthesis in the isolated toad urinary bladder. PGE apparently is not the metabolite responsible for the increase in SCC.