Université Paris-Sud 11, Faculté de Médecine, 94276 Kremlin-Bicêtre, France, AP-HP, Centre de Référence de l’Hypertension Pulmonaire Sévère, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine Béclère, 92140 Clamart, France, Inserm U999, IPSIT, LabEx LERMIT, Centre Chirurgical Marie-Lannelongue, 92350 Le Plessis-Robinson, France, AP-HP, Service de Pharmacie, Hôpital Antoine Béclère, 92140 Clamart, France, Université Paris-Sud 11, Faculté de Pharmacie, 92290 Châtenay-Malabry, France, Laboratoire d’Analyses Biomédicales, Centre Chirurgical Marie-Lannelongue, 92350 Le Plessis-Robinson, France
Pulmonary hypertension (PH) is defined as an increase in mean pulmonary arterial pressure above 25 mmHg. Pulmonary vasoconstriction, cellular proliferation, inflammation, and oxidative stress are involved in the pathophysiology of PH. Since hypomagnesemia was reported to promote endothelial cell dysfunction leading to inflammation and oxidative stress, we investigated the potential involvement of magnesium (Mg) deficiency in experimental and human PH. Our results indicate that Mg deficiency has no impact on hypoxia-induced PH development or severity, and that no reduction in Mg plasma concentration was observed in patients with severe pulmonary arterial hypertension. Thus, hypomagnesemia does not appear to play a role in the pathophysiology of experimental and human pulmonary hypertension.