Magnesium decreases arterial pressure and inhibits cardiovascular responses induced by N-methyl-D-aspartate and metabotropic glutamate receptors stimulation in rostral ventrolateral medulla

Objective: Magnesium sulfate (MgSO₄) is widely used for the treatment of eclampsia. However, effects of Mg²⁺ in central cardiovascular regulation remain unclear. In the present study, the role of Mg²⁺ on cardiovascular regulation in the rostral ventrolateral medulla (RVLM) of rats was examined. Methods: Adult male Wistar rats were anesthetized with urethane, and artificially ventilated. The ventral surface of the medulla was exposed, and the RVLM was identified by microinjection (50 nl) of L-glutamate (L-Glu; 2 nmol). Then, MgSO₄ (1, 3, 10 nmol, n = 7 for each dose) and magnesium chloride (MgCl₂; 10 nmol, n = 7) were microinjected into the RVLM. L-Glu (2 nmol), N-methyl-D-aspartate (NMDA; 20 pmol), α-amino-3-hydroxy-5-methyl isoxazole-4-propionic acid (AMPA; 5 pmol) and (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD, metabotropic glutamate receptor agonist; 1 nmol] were also microinjected with or without pretreatment of MgSO₄ (10 nmol; n = 7 for each drug). Results: MgSO₄ dose-dependently decreased mean arterial pressure (MAP) and heart rate (HR). The high dose of MgSO₄ (10 nmol) significantly decreased MAP and HR (-25 ± 4 mmHg and -43 ± 6 bpm). Similarly, MgCl₂ decreased MAP and HR (-27 ± 4 mmHg and -30 ± 6 bpm). The pressor response evoked by NMDA or (1S,3R)-ACPD was significantly attenuated by the pretreatment with MgSO₄. In contrast, pressor response caused by L-Glu or AMPA was not affected by pretreatment with MgSO₄. Conclusions: These results suggest that Mg²⁺ has an inhibitory role on the RVLM neurons, and inhibits cardiovascular responses induced by NMDA and metabotropic glutamate receptor agonists.