Role of potassium channels in fetal loss and maternal cardiovascular dysfunction during pregnancy
Our lab focuses on the influence of the small conductance Ca2+-activated K+ (SK3) channel on vascular remodeling at the maternal-fetal interface during pregnancy. During pregnancy, the maternal cardiovascular system must adapt to accommodate the needs of the developing fetus. Pathological conditions that compromise the ability of the maternal cardiovascular system to adapt and remodel are associated with pregnancy complications including growth restriction, preterm delivery and fetal demise. However, the basic mechanisms that underlie maternal cardiovascular adaptations and how their dysfunction translates into poor fetal outcomes are not completely understood. The relationship between maternal cardiovascular regulation and pregnancy complications is central to improving fetal outcomes.
Recent evidence indicates that K+ channels contribute to vascular remodeling and are targets for pregnancy-related vascular diseases. However, their role in fetal outcomes is unknown. The SK3 channel is present in vascular endothelial cells, and non-pregnant transgenic mice that overexpress the SK3 channel (SK3T/T) have an increase in uterine artery diameter. Our laboratory has found that in SK3T/T mice have an increased incidence of fetal demise, intrauterine growth restriction, and elevated angiogenic factors. Our projects are focused on establishing how maternal SK3 channel expression impacts cardiovascular adaptations during pregnancy and fetal outcomes and identifying the mechanism by which overexpression of the SK3 channel leads to fetal demise. A better understanding of mechanisms that regulate maternal adaptation during pregnancy will provide a basis for improving maternal and fetal outcomes.