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Mg affects vascular smooth muscle contraction by direct and endothelium-dependent pathways. The major mechanism of endothelium-dependent relaxation (EDR) in resistance arteries is independent of nitric oxide synthase and cyclooxygenase and mediated by Ca-activated K channels (sK and iK). We tested the effect of modified extracellular Mg (Mge) concentration upon this mechanism, in isolated small mesenteric arteries from rat. EDR was induced by carbachol 10 10 M, in rings contracted by phenylephrine 10 M, in the presence of N(G)-Nitro-L-arginine methyl ester (L-NAME) 10 M and indomethacin 10 M, with [Mge] kept at 2, 1.2, or 0.8 mM. This EDR is enhanced by high [Mge] and reduced by low [Mge], vs. the one in regular [Mge] of 1.2 mM (n = 6; p < 0.01). Mge similarly modulates relaxation induced by SKA-31 (sK/iK activator). These new Mge actions do not involve known Mg effects on sK/iK and may be relevant in Mg therapy.

EXTRACELLULAR MG2+ LEVEL AFFECTS THE MAJOR MECHANISM OF ENDOTHELIUM-DEPENDENT RELAXATION IN RESISTANCE ARTERIES