Fig. 1. The potential role of pregnancy and hypoxia in regulation of K⁺ channels in uterine vasculatures.

Activation of protein kinase C (PKC) results in inhibition of K⁺ channels activity. The increased sex steroid hormones/their receptors during pregnancy down-regulate PKC gene expression and/or activity in uterine artery smooth muscle cells, which leads to a selectively increased K⁺ channels expressions and activities in uterine vasculatures during pregnancy. However, chronic hypoxia during pregnancy enhances PKC activity via down-regulation of steroid hormone-mediated signaling, resulting in decreased K⁺ channels activities and increased uterine vascular tone.