Ca2+-Activated K+ Channels and the Regulation of the Uteroplacental Circulation

Adequate uteroplacental blood supply is essential for the development and growth of the placenta and fetus during pregnancy. Aberrant uteroplacental perfusion is associated with pregnancy complications such as preeclampsia, fetal growth restriction (FGR), and gestational diabetes. The regulation of uteroplacental blood flow is thus vital to the well-being of the mother and fetus. Ca2+-activated K+ (K-Ca) channels of small, intermediate, and large conductance participate in setting and regulating the resting membrane potential of vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) and play a critical role in controlling vascular tone and blood pressure. K-Ca channels are important mediators of estrogen/pregnancy-induced adaptive changes in the uteroplacental circulation. Activation of the channels hyperpolarizes uteroplacental VSMCs/ECs, leading to attenuated vascular tone, blunted vasopressor responses, and increased uteroplacental blood flow. However, the regulation of uteroplacental vascular function by K-Ca channels is compromised in pregnancy complications. This review intends to provide a comprehensive overview of roles of K-Ca channels in the regulation of the uteroplacental circulation under physiological and pathophysiological conditions.

Automated summary

Adequate uteroplacental blood supply is crucial for the development and growth of the placenta and fetus during pregnancy. The regulation of uteroplacental blood flow, controlled by Ca2+-activated K+ (K-Ca) channels, is vital for the well-being of the mother and fetus. However, the regulation of uteroplacental vascular function by K-Ca channels is compromised in pregnancy complications. This review provides a comprehensive overview of the roles of K-Ca channels in the regulation of the uteroplacental circulation under physiological and pathophysiological conditions.