Endothelium-dependent influence of small changes in extracellular magnesium concentration on the tone of feline middle cerebral arteries.

Abstract

The aim of this study was to investigate the effect of small alterations in the extracellular magnesium concentration on the tone of feline middle cerebral arteries and to examine the role of the endothelium in these responses. We measured the isometric tension of isolated arterial rings placed between two stainless steel wires in a tissue chamber containing Krebs-Henseleit solution aerated with a gas mixture containing 95% O 2 and 5% CO 2 at 37°C. After precontraction with noradrenaline, a decrease of the extracellular magnesium concentration from 1.2 mM to 1.0 and 0.8 mM resulted in sustained relaxations, whereas elevation of the extracellular magnesium concentration from 0.8 mM to 1.2 mM caused an increase in vascular tone when the endothelium was intact The magnesium deficiency-related dilations were absent in endothelium-denuded vessels and were inhibited by 5 x 10"' M oxyhemoglobin and 1 0 s M methylene blue, suggesting the involvement of an endothelium-derived relaxing factor in this vascular response. However, 5 x l 0~7 M nifedipine or 3xlO~s M dichlorobenzamil did not affect the magnesium deficiency-related relaxations. Therefore, nifedipine-sensitive calcium channels or the sodium/calcium antiport system are not involved in this vascular action of magnesium. We conclude that small alterations in the extracellular magnesium concentration, possibly within the physiological range, are able to modify the basal formation and release of endotheliumderived relaxing factor and thus alter arterial smooth muscle tone in this vascular bed. This endothelium-and magnesium-dependent system appears to be more sensitive than the direct smooth muscle actions of magnesium and might exert a protective effect against magnesium deficiency-induced direct cerebrovascular contraction. (Stroke 1991;22:785-789)

Magnesium Removal Impairs the Regulatory Role of Rat Endothelium.

“…The facts seem to be incompatible with the reports that (27,28). Indeed, an acute decrease in extracellular Mg results in a transient relaxation followed by a sustained contraction in arteries with intact endothelium (29)(30)(31). It is possible that an increase in calcium influx caused by Mg removal may be transient and, therefore, the response by the release of EDRF cannot be detected in the present experimental condition where external Mg was removed 30 min before the addition of norepinephrine.…”

Low Serum Magnesium Predicts Neurological Events in Patients With Advanced Atherosclerosis

“…A direct relation between serum Mg levels and acute neurological events has not yet been described. However, Mg has been demonstrated to coregulate cerebrovascular smooth muscle tone, 14 and low serum Mg was associated with the development of cerebrovascular atherosclerosis. 6,7 There is some evidence supporting the hypothesis that dietary Mg intake potentially contributes to blood pressure and stroke reduction.…”

Assessment of the effects of endothelin‐1 and magnesium sulphate on regional blood flows in conscious rats, by the coloured microsphere reference technique

“…There is evidence to suggest that magnesium (Mg 2+ ) is bene®cial in the treatment of a number of conditions, including pre-eclampsia (Lucas et al, 1995;Eclampsia Trial Collaborative Group, 1995) and acute myocardial infarction (Woods et al, 1992). The mode of action of Mg 2+ in these conditions is not clear, although vasodilator properties of Mg 2+ are well documented both in vitro (Altura & Altura, 1980Altura & Turlapaty, 1981;Kimura et al, 1989;Skajaa et al, 1990;Szabo et al, 1991Szabo et al, , 1992Noguera & D'Ocon, 1993), and in vivo (Seelig et al, 1983;Dipette et al, 1987;Nishio et al, 1989;Chi et al, 1990;Ram et al, 1991;Sipes et al, 1991;Perales et al, 1991;Kemp et al, 1993Kemp et al, , 1994. Woods (1991) suggested that Mg 2+ is a coronary vasodilator, and that some of the bene®cial eect of Mg 2+ in the treatment of acute myocardial infarction may be due to the prevention and relief of coronary vasospasm associated with the condition.…”