Ebeigbe A B, Aloamaka C P
Res Exp Med (Berl). 1987;187(1):25-31. doi: 10.1007/BF01854965.
The role of endothelium in the relaxation of rat aortic smooth muscle to raised extracellular magnesium concentration (Mg2+)o has been examined. Following contractile responses to norepinephrine (NE) or high-K+ in Mg2+-free media, cumulative increases in (Mg2+)o caused concentration-dependent relaxations in intact (+E) as well as endothelium-denuded (-E) strips. In NE-stimulated strips, Mg2+-induced relaxation was significantly greater in +E strips, whereas the reverse was the case in K+-stimulated strips. Bay K8644, a Ca2+ channel agonist, did not modify Mg2+-induced relaxation in NE-stimulated strips, but significantly attenuated the relaxation in K+-stimulated strips in the order: -E greater than +E. The results suggest that Mg2+-induced relaxation of rat aorta is associated, at least in part, with the release of an endothelium-derived relaxant factor in receptor-mediated, but not in depolarisation-dependent contractions.
研究了内皮在大鼠主动脉平滑肌对细胞外镁离子浓度（Mg2+）o升高的舒张反应中的作用。在无镁培养基中对去甲肾上腺素（NE）或高钾产生收缩反应后，细胞外镁离子浓度（Mg2+）o的累积增加导致完整（+E）和去内皮（-E）血管条出现浓度依赖性舒张。在NE刺激的血管条中，镁离子诱导的舒张在+E血管条中明显更大，而在钾离子刺激的血管条中情况则相反。钙通道激动剂Bay K8644不会改变NE刺激的血管条中镁离子诱导的舒张，但会按-E大于+E的顺序显著减弱钾离子刺激的血管条中的舒张。结果表明，镁离子诱导的大鼠主动脉舒张至少部分与内皮源性舒张因子的释放有关，该释放发生在受体介导的收缩中，而非去极化依赖性收缩中。
