Why the study?
Does the removal of extracellular magnesium ions inhibit acetylcholine-induced endothelium-dependent relaxation in isolated canine coronary arteries?
Does the removal of extracellular magnesium ions inhibit acetylcholine-induced endothelium-dependent relaxation in isolated canine coronary arteries?
Extracellular magnesium is an important co-factor for acetylcholine-induced endothelium-dependent relaxation in canine coronary arteries, suggesting a potential role for magnesium deficiency in the etiology of coronary vasospasm.
Magnesium deficiency may promote coronary vasospasm; hypothesis-generating in canine arteries and requires human validation.
A great deal of interest has recently focused upon the mechanism(s) associated with the generation and action of endothelium-derived relaxant factors (EDRFs) in blood vessels. Since we have shown that extracellular magnesium ions ([Mg2+]o) are important in control of coronary vascular tone and reactivity, we wondered whether these divalent cations play any role in the generation or action of EDRF in coronary arterial smooth muscle. Using isolated canine coronary arterial rings, we have now found that removal of [Mg2+]o inhibits the ability of these vascular preparations to relax when challenged with acetylcholine; in the absence of [Mg2+]o, the relaxation concentration-response curves for acetylcholine are shifted markedly to higher concentrations with small maxima. It, thus, appears that [Mg2+]o is an important co-factor for acetylcholine-induced endothelium-dependent relaxation in canine coronary arteries. These findings support our previous hypothesis that dietary deficiency of Mg may be an important factor in aetiology of coronary vasospasm.
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Altura et al. (1987) studied this question.
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