镁/钙对猪睫状动脉中内皮素-1诱导的收缩的调节作用
Modulation of endothelin-1-induced contractions by magnesium/calcium in porcine ciliary arteries.
作者信息
Dettmann E S, Lüscher T F, Flammer J, Haefliger I O
机构信息
Laboratory of Ocular Pharmacology and Physiology, University Eye Hospital Basel, Switzerland.
出版信息
Graefes Arch Clin Exp Ophthalmol. 1998 Jan;236(1):47-51. doi: 10.1007/s004170050041.
BACKGROUND
The present study was performed to investigate the influence of extracellular magnesium on changes in contractile tone induced by endothelin-1, and on relaxations to bradykinin in isolated porcine ciliary arteries.
METHODS
Vessels were studied in a myograph system for measurement of isometric forces. Concentration-response curves (10(-10)-10(-7) M) to endothelin-1 were constructed in the presence of different concentrations (0, 1.2, 2, 10 mM) of magnesium (MgSO4). Endothelin-1-precontracted vessels (approximately 10(-8) M) were exposed to magnesium (10(-5)-10(-2) M) in the presence or absence of either the inhibitor of nitric oxide formation L-NAME (approximately 10(-4) M), or different concentrations of calcium (2.5, 5, 10 mM). In endothelin-1-precontracted vessels (10(-8) M), relaxations to bradykinin (10(-10)-10(-6) M) were conducted in the presence of different concentrations of magnesium (0, 1.2, 10 mM).
RESULTS
Contractions to endothelin-1 were reduced only in the presence of 10 mM magnesium. (1.2 mM vs 10 mM, P = 0.001). In endothelin-1-precontracted vessels, magnesium evoked complete concentration-dependent relaxations (pD2 = 3.1 +/- 0.1), which were shifted to the right by increasing extracellular concentrations of calcium (2.5 vs 5 mM, P < 0.05). L-NAME had no influence on magnesium-induced relaxations. Relaxations to bradykinin remained unaffected by changes in extracellular magnesium concentrations.
CONCLUSIONS
In a mechanism which appears to be compatible with a calcium-antagonist effect, magnesium strongly modulates changes in contractile tone evoked by endothelin-1, but has no effect on bradykinin-induced relaxations.
背景
本研究旨在探讨细胞外镁对内皮素-1诱导的收缩张力变化以及对离体猪睫状动脉中缓激肽舒张作用的影响。
方法
在肌动描记系统中研究血管，以测量等长力。在不同浓度（0、1.2、2、10 mM）的镁（硫酸镁）存在下构建内皮素-1的浓度-反应曲线（10⁻¹⁰ - 10⁻⁷ M）。在存在或不存在一氧化氮生成抑制剂L-NAME（约10⁻⁴ M）或不同浓度钙（2.5、5、10 mM）的情况下，将内皮素-1预收缩的血管（约10⁻⁸ M）暴露于镁（10⁻⁵ - 10⁻² M）。在内皮素-1预收缩的血管（10⁻⁸ M）中，在不同浓度的镁（0、1.2、10 mM）存在下进行对缓激肽（10⁻¹⁰ - 10⁻⁶ M）的舒张实验。
结果
仅在10 mM镁存在时，对内皮素-1的收缩作用减弱（1.2 mM与10 mM相比，P = 0.001）。在内皮素-1预收缩的血管中，镁引起完全的浓度依赖性舒张（pD2 = 3.1 ± 0.1），随着细胞外钙浓度增加（2.5 mM与5 mM相比，P < 0.05），舒张曲线右移。L-NAME对镁诱导的舒张无影响。细胞外镁浓度的变化对缓激肽诱导的舒张无影响。
结论
在一种似乎与钙拮抗剂作用相符的机制中，镁强烈调节内皮素-1引起的收缩张力变化，但对缓激肽诱导的舒张无作用。
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