Mechanisms modulating estrogen-induced uterine vasodilation

Estrogen, a potent vasodilator, has its greatest effects in reproductive tissues, e.g., increasing uterine blood flow (UBF) 5- to 10-fold within 90 min after a bolus dose. High-conductance potassium channels and nitric oxide (NO) contribute to the uterine responses, but other factors may be involved. We examined the role of ATP-dependent (ATP-sensitive) and voltage-gated (K v) potassium channels and new protein synthesis in ovariectomized ewes with uterine artery flow probes, infusing intraarterial inhibitors glibenclamide (GLB; K ATP), 4-aminopyridine (4-AP; K v) or cycloheximide, respectively, into one uterine horn before and/or after systemic estradiol-17β (E 2β, 1 μg/kg iv). E 2β alone increased UBF >5-fold and heart rate by 10–25% ( P