Placental protein 13 dilation of pregnant rat uterine vein is endothelium dependent and involves nitric oxide/calcium activated potassium channels signals

Introduction: Accumulating evidence demonstrates the importance of the galectin protein Placental Protein 13 (PP13) in predicting Preeclampsia (PE), a gestational disorder that has no cure and is associated with a compromised uterine vascular adaptation to pregnancy. Uterine vasculature undergoes significant remodeling (growth in length and in circumference) during normal pregnancy to accommodate the increased blood volume to the feto-placental unit. The aim of this study was to demonstrate the role of PP13 on the uterine veins (UVs).Methods: PP13 was tested on UVs isolated from rat by using a pressurized myograph. The PP13 investigation was carried out in the presence of: a) nitric oxide synthases inhibitors (L-NAME + L-NNA, 2 x 10(-4) M); b) small conductance Ca2+-activated K+ channels (SKca) inhibitor (Apamin, 10(-7) M); c) intermediate conductance Ca(2+)activated K+ channels (IKca) inhibitor (TRAM-34, 10(-5) M); d) big conductance Ca2+-activated K+ channels (BKca) inhibitor (Paxilline, 10(-5) M) and in the absence of endothelium.Results: Our results showed that in late pregnancy, PP13 induced a significant dilation of UVs that is endothelium dependent. Further, PP13-dilation is mediated by the SKca - NO - BKca pathway.Discussion: For the first time, this study provides evidence that in pregnancy, the UVs are dilated by PP13 and suggests SKCa as a potential target for treatments aimed at restoring pregnancy complication associated with deficiency in uterine adaptation.