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% O2 and 5% CO2 at 37 degrees 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(-6) M
oxyhemoglobin and 10(-5) M
methylene blue, suggesting the involvement of an
endothelium-derived relaxing factor in this vascular response. However, 5 x 10(-7)
M nifedipine or 3 x 10(-5) 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
endothelium-derived relaxing factor and thus alter arterial smooth muscle tone in this vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)