86 MgSO4 modulates A2A and A2B adenosine receptors, eNOS and iNOS expression, and l-arginine transport in human placental microvascular endothelial cells : Magnesium sulphate

Control of vascular tone in the human placenta depends on locally-generated endothelium derived vasoactive molecules. Nitric oxide (NO) is a vasodilator that caused low impedance, high-blood flow circuit facilitating the transfer of oxygen and other nutrients to the developing fetus. Thus, molecules that regulate the synthesis or bioavailability of NO are determinant in this phenomenon. The cationic amino acid l-arginine is the substrate for NO synthases (NOS) and NOS activity seems dependent on the l-arginine transport at the plasma membrane in endothelial cells. The endogenous nucleoside adenosine activates l-arginine transport and NO synthesis in the foetoplacental endothelium via activation of A2A adenosine receptors (A2AAR) in normal pregnancies. Interestingly, maternal foetal plasma concentration of adenosine is increased in preeclampsia, a syndrome associated with reduced vascular reactivity and blood flow. Since magnesium (Mg2+) is required for A2AAR-dependent dilation of rat mesenteric vessels, a potential link between Mg2+ and adenosine receptors in the foetoplacental vasculature is likely. We hypothesize that human placental microvascular endothelial cells (hPMECs) show increased A2AR expression and l-arginine transport when exposed to MgSO4.