Calcium-activated potassium channels and nitric oxide coregulate estrogen-induced vasodilation

1 Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390; and 2 Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912 Nitric oxide synthase (NOS) contributes to estradiol-17 (E 2 )-induced uterine vasodilation, but additional mechanisms are involved, and the cellular pathways remain unclear. We determined if 1 ) uterine artery myocytes express potassium channels, 2 ) E 2 activates these channels, and 3 ) channel blockade plus NOS inhibition alters E 2 -induced uterine vasodilation. Studies of cell-attached patches identified a 107 ± 7 pS calcium-dependent potassium channel (BK Ca ) in uterine artery myocytes that rapidly increased single-channel open probability 70-fold ( P