Vasopressin-stimulated water flow is decreased by thromboxane synthesis inhibition or antagonism.
The time course of vasopressin stimulation of water flow and immunoreactive thromboxane B2 (iTXB2) and prostaglandin E (iPGE) biosynthesis was studied in the isolated toad urinary bladder. Vasopressin (25 mU/ml) significantly stimulated iTXB2 synthesis within 8 min, synthesis reaching a maximum rate by 17 min. iPGE synthesis was significantly stimulated within 8 min, remaining unchanged for 24 min. Maximum vasopressin-stimulated water flow was reached between 16 and 24 min. 7-(1-Imidazolyl)-heptanoic acid (7IHA), a thromboxane synthetase inhibitor, inhibited both vasopressin-stimulated water flow and iTXB2 synthesis in a dose-dependent fashion, but did not affect iPGE synthesis. Vasopressin-stimulated water flow and iTXB2 synthesis were significantly correlated (r = 0.75, n = 24, P less than 0.001). 13-Azaprostanoic acid (13APA), a thromboxane antagonist, inhibited vasopressin-stimulated water flow in a dose-dependent fashion. Inhibition of arachidonic acid metabolism abolished the effects of 7IHA and 13APA on vasopressin-stimulated water flow. 7IHA and 13APA had no effect on cAMP-stimulated water flow. These results confirm that vasopressin stimulates TXA2 and PGE synthesis and support the hypothesis that TXA2 is a positive modulator of vasopressin-stimulated water flow in the toad urinary bladder.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism*; D002024:Bufo marinus / Q000378:metabolism; D006538:Heptanoic Acids / Q000494:pharmacology; D066298:In Vitro Techniques; D011458:Prostaglandins E / Q000096:biosynthesis*; D011466:Prostanoic Acids / Q000494:pharmacology; D013268:Stimulation, Chemical; D001743:Urinary Bladder / Q000378:metabolism*; D014667:Vasopressins / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D014867:Water / Q000378:metabolism*
D001095:Arachidonic Acids; D006538:Heptanoic Acids; D011458:Prostaglandins E; D011466:Prostanoic Acids; D014867:Water; D014667:Vasopressins