Background: Magnesium sulfate (MgSO4) has been used as a common therapy for preeclampsia and eclampsia for many years. MgSO4 decreases peripheral vascular resistance so as to reduce maternal blood pressure. Whether placental blood vessels react to MgSO4 in the same patterns as that in maternal vessels is largely unknown.
Methods and results: This study compared placental vessels (PV) versus nonplacental vessels (non-PV) in human and animal models. MgSO4-caused vascular dilation was significantly weaker in PV than that in non-PV. Prostaglandin I2 synthetase affected MgSO4-mediated vasodilatation in PV, not in umbilical vessels, while cyclooxygenase did not influence MgSO4-induced relaxation in both PV and non-PV. Mg2+-caused vasodilatation was mainly through calcium channels. In PV, calcium channel activities were significantly weaker in PV than that in non-PV. Relative mRNA expression of CACNA1D, CACNB2, and CACNB3 was significantly higher in PV than those in umbilical vessels, despite the fact that the expression of CACNA1F was less in PV. The contractile phenotype of smooth muscle cell marker (CALD1) was less and the synthetic phenotype (MYH10) was more in PV than that in UV.
Conclusions: These results demonstrated that PV were characterized by much weaker responses to MgSO4 compared with nonplacental vessels. The difference was related to weaker calcium channel activity and minor contractile phenotype smooth muscle cells in PV, providing important information for further understanding treatments with MgSO4 in preeclampsia.
Keywords: MgSO4; calcium channel; nonplacental vessels; placental vessels; preeclampsia/pregnancy; vasodilation.
© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.