Macdonald P S, Dubbin P N, Dusting G J
Clin Exp Pharmacol Physiol. 1986 Apr;13(4):335-40. doi: 10.1111/j.1440-1681.1986.tb00359.x.
Vasodilator responses were examined in bovine coronary artery rings preconstricted with the thromboxane-mimetic, U46619. A23187 produced endothelium-dependent vasodilatation that was abolished in calcium-free solution. In contrast, endothelium-dependent vasodilatation produced by arachidonic acid was not altered in calcium-free solution. In calcium-free solution, indomethacin (10 mumol/l) did not affect arachidonate-induced relaxations whereas BW755C (100 mumol/l) reduced relaxations to low concentrations of arachidonate, and proadifen (SKF-525A, 1 mmol/l) abolished them at all concentrations. Endothelium-independent relaxations produced by glyceryl trinitrate were not affected by proadifen (1 mmol/l). It is clear that arachidonic acid bypasses a calcium-dependent step in the release of endothelium-derived relaxing factor, perhaps acting as an intermediate precursor. The data support the hypothesis that a cytochrome P-450 mono-oxygenase may also be involved.
在用血栓素类似物U46619预收缩的牛冠状动脉环中检测血管舒张反应。A23187产生内皮依赖性血管舒张,在无钙溶液中这种舒张作用消失。相比之下,花生四烯酸产生的内皮依赖性血管舒张在无钙溶液中未改变。在无钙溶液中,吲哚美辛(10 μmol/L)不影响花生四烯酸诱导的舒张,而BW755C(100 μmol/L)降低了对低浓度花生四烯酸的舒张反应,丙胺卡因(SKF - 525A,1 mmol/L)在所有浓度下均消除了这种舒张反应。硝酸甘油产生的非内皮依赖性舒张不受丙胺卡因(1 mmol/L)影响。显然,花生四烯酸绕过了内皮源性舒张因子释放过程中依赖钙的步骤,可能作为一种中间前体起作用。这些数据支持细胞色素P - 450单加氧酶也可能参与其中的假说。