Open AccessMagnesium Sulfate–Mediated Vascular Relaxation and Calcium Channel Activity in Placental Vessels Different From Nonplacental Vessels
Author(s) -
Tang Jiaqi,
He Axin,
Li Na,
Chen Xueyi,
Zhou Xiuwen,
Fan Xiaorong,
Liu Yanping,
Zhang Mengshu,
Qi Linglu,
Tao Jianying,
Sun Miao,
Xu Zhice
Publication year - 2018
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.118.009896
Subject(s) - medicine , vasodilation , vascular smooth muscle , calcium , blood vessel , preeclampsia , endocrinology , calcium channel , magnesium , smooth muscle , pregnancy , biology , chemistry , organic chemistry , genetics
Background Magnesium sulfate (Mg SO 4 ) has been used as a common therapy for preeclampsia and eclampsia for many years. Mg SO 4 decreases peripheral vascular resistance so as to reduce maternal blood pressure. Whether placental blood vessels react to Mg SO 4 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. Mg SO 4 ‐caused vascular dilation was significantly weaker in PV than that in non‐ PV . Prostaglandin I 2 synthetase affected Mg SO 4 ‐mediated vasodilatation in PV , not in umbilical vessels, while cyclooxygenase did not influence Mg SO 4 ‐induced relaxation in both PV and non‐ PV . Mg 2+ ‐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 CACNA 1D , CACNB 2 , and CACNB 3 was significantly higher in PV than those in umbilical vessels, despite the fact that the expression of CACNA 1F was less in PV . The contractile phenotype of smooth muscle cell marker ( CALD 1) was less and the synthetic phenotype ( MYH 10) was more in PV than that in UV . Conclusions These results demonstrated that PV were characterized by much weaker responses to Mg SO 4 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 Mg SO 4 in preeclampsia.