Prostaglandin-induced activation of uterine contractility in pregnant rats does not involve potassium channels

OBJECTIVE: The uterus is a target for prostaglandins, especially at the end of gestation. Whether potassium channels are involved in the effect of prostaglandins is not clear. The aim of this study was to find out. STUDY DESIGN: Concentration-response relationships to prostaglandins (prostaglandin F2α, prostaglandin E2, and prostaglandin I2 [carbacyclin]; 10−10 mol/L-10−4 mol/L) were studied in isolated uterine rings from mid pregnancy (day 14) and late pregnancy (day 21) rats (Krebs solution, 5% CO2in air, 37°C; pH, 7.4). Rings were incubated for 30 minutes with either solvent or adenosine triphosphate-sensitive potassium channel inhibitor or opener glibenclamide and levcromakalim or with calcium-sensitive potassium channel inhibitor or opener NS1619 and iberiotoxin, respectively. The changes in integral activity were compared after each concentration of the agent and were expressed as a percent of the basal integral activity. RESULTS: The increases in spontaneous contractile activity induced by prostaglandin E2 and carbacyclin, but not prostaglandin F2α, were statistically significantly higher in tissues from late pregnancy versus mid pregnancy rats and were not affected by any of the K-channel openers or inhibitors. CONCLUSION: Adenosine triphosphate-sensitive and calcium-sensitive potassium channels are not involved in the effect of prostaglandin F2α, prostaglandin E2, and prostaglandin I2 on pregnant rat uterus. (Am J Obstet Gynecol 2002;186:453-7.)