Szabó C, Faragó M, Dóra E, Horváth I, Kovách A G
Experimental Research Department, Semmelweis University Medical School, Budapest, Hungary.
Stroke. 1991 Jun;22(6):785-9. doi: 10.1161/01.str.22.6.785.
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)
本研究的目的是探讨细胞外镁浓度的微小变化对猫大脑中动脉张力的影响,并研究内皮在这些反应中的作用。我们在一个组织浴槽中测量置于两根不锈钢丝之间的离体动脉环的等长张力,该组织浴槽中含有用含95% O₂和5% CO₂的混合气体在37℃下曝气的Krebs-Henseleit溶液。在用去甲肾上腺素预收缩后,细胞外镁浓度从1.2 mM降至1.0 mM和0.8 mM会导致持续舒张,而当内皮完整时,细胞外镁浓度从0.8 mM升至1.2 mM会引起血管张力增加。内皮剥脱的血管中不存在与镁缺乏相关的舒张,且5×10⁻⁶ M氧合血红蛋白和10⁻⁵ M亚甲蓝可抑制这种舒张,提示内皮源性舒张因子参与了这种血管反应。然而,5×10⁻⁷ M硝苯地平或3×10⁻⁵ M二氯苯甲酰胺并不影响与镁缺乏相关的舒张。因此,硝苯地平敏感的钙通道或钠/钙反向转运系统不参与镁的这种血管作用。我们得出结论,细胞外镁浓度的微小变化,可能在生理范围内,能够改变内皮源性舒张因子的基础生成和释放,从而改变该血管床的动脉平滑肌张力。(摘要截断于250字)