Hashimoto M, Ishida Y, Sakuma I, Tanaka Y, Masumura S
Department of Physiology, Shimane Medical University, Izumo, Japan.
Life Sci. 1994;54(8):525-31. doi: 10.1016/0024-3205(94)90002-7.
Intact and rubbed coronary arteries responded to acetylcholine (ACh) with contractions in a cumulative dose-dependent manner. The rubbed artery contracted at a lower concentration of ACh (3 x 10(-8) M) than the threshold level of the agonist in the intact artery (10(-7) M). Only in the intact artery was the second cumulative dose-response to ACh (10(-6) M) decreased by 60% (p < 0.05). Pretreatment of the intact artery with methylene blue or NG-monomethyl-L-arginine (L-NMMA) increased the contractile response to ACh. The ACh-induced increase of the cGMP level in the intact artery was eliminated by removal of the endothelial cells and by pretreatment of the artery with either methylene blue or L-NMMA. These findings indicate that the endothelial cells in the coronary artery are responsible for the ACh-induced relaxation, presumably mediated by an endothelium-derived relaxing factor.
完整的冠状动脉和经摩擦处理的冠状动脉对乙酰胆碱(ACh)的反应呈累积剂量依赖性收缩。经摩擦处理的动脉在较低浓度的ACh(3×10⁻⁸ M)时发生收缩,而完整动脉中激动剂的阈值浓度为10⁻⁷ M。仅在完整动脉中,对ACh(10⁻⁶ M)的第二次累积剂量反应降低了60%(p<0.05)。用亚甲蓝或N-单甲基-L-精氨酸(L-NMMA)预处理完整动脉可增强对ACh的收缩反应。去除内皮细胞以及用亚甲蓝或L-NMMA预处理动脉可消除ACh诱导的完整动脉中cGMP水平的升高。这些发现表明,冠状动脉中的内皮细胞负责ACh诱导的舒张,推测是由内皮衍生的舒张因子介导的。