Inhibition of vasopressin-stimulated prostaglandin E biosynthesis by chlorpropamide in the toad urinary bladder. Mechanism of enhancement of vasopressin-stimulated water flow.
Chlorpropamide is known to enhance the water permeability response of the toad urinary bladder to vasopressin and to theophylline. In other studies, we have shown that prostaglandin E synthesis by the toad bladder inhibits the water permeability response to arginine vasopressin and to theophylline. In this study, the effect of chlorpropamide on vasopressin-, theophylline-, and cyclic AMP-stimulated water flow and on prostaglandin E biosynthesis was investigated in the toad urinary bladder in vitro. Chlorpropamide inhibited prostaglandin E biosynthesis during vasopressin-, theophylline- and cyclic AMP-stimulated water flow. Tolbutamide and glyburide, two other sulfonylurea compounds, also enhanced vasopressin-stimulated water flow and inhibited vasopressin-stimulated prostaglandin E biosynthesis. We conclude that the mechanism of enhancement on vasopressin-stimulated water flow by the sulfonylureas is the inhibition of prostaglandin E biosynthesis.
D000818:Animals; D001001:Anura; D001127:Arginine Vasopressin / Q000494:pharmacology*; D002747:Chlorpropamide / Q000494:pharmacology*; D002855:Chromatography, Thin Layer; D000242:Cyclic AMP / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D050356:Lipid Metabolism; D010539:Permeability; D011458:Prostaglandins E / Q000096:biosynthesis*; D013268:Stimulation, Chemical; D013329:Structure-Activity Relationship; D013806:Theophylline / Q000494:pharmacology; D014044:Tolbutamide / Q000494:pharmacology; D001743:Urinary Bladder / Q000378:metabolism*; D014667:Vasopressins / Q000031:analogs & derivatives*; D014867:Water / Q000378:metabolism*
D011458:Prostaglandins E; D014867:Water; D014667:Vasopressins; D001127:Arginine Vasopressin; D014044:Tolbutamide; D013806:Theophylline; D000242:Cyclic AMP; D005905:Glyburide; D002747:Chlorpropamide