Regulation of smooth muscle contractility is crucial aspect of uterine physiology. This is highlighted by the developmental switch that the myometrium undergoes as gestation progresses into labour. However, little is known about the molecular mechanisms that govern the change in contractile phenotype and how these mechanisms are affected in pathological scenarios. Potassium channels are integral to the control of myometrial contraction and various types of potassium channel have been identified in rodent and human myometrial smooth muscle. Our collaborative work has focussed upon the expression and functional impact of two types of voltage-gated potassium channels previously associated with neuronal and cardiac excitability namely KCNQ- and ether-a-go-go (KCNH) genes. This talk will be give an overview of our work on these channels showing the expression of different KCNQ and KCNH isoforms in uterus from non-pregnant and pregnant animals as well as human tissues. It will also highlight the different impact of these potassium channels in myometrial contractility with ERG channels losing functional impact as gestation develops whereas KCNQ channels remain a robust and therapeutically viable target through-out pregnancy. These data have provided mechanistic insight into uterine physiology and provide new possible targets for therapeutic intervention.