Abstract

Much research has been undertaken to define what determines the inherent contractility of the myometrial smooth muscle and what dictates the switch from relaxed to contractile phenotype. While a lot has been deciphered the fundamental mechanisms that initiate and maintain the switch in uterine physiology are ill defined. Uterine physiology is indubitably complex so this article focuses on one piece of the puzzle: the role of certain potassium channels in determining myometrial contractility and how altered activity may contribute to the hyper-contractile uterus at term.