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 Ca2+-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.
Keywords: Ca(2+)-activated K(+) channels: (SK(ca), IK(ca), BK(ca)); PP13; Uterine vascolature; Vasodilation.
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