Watson E L
Eur J Pharmacol. 1978 Nov 15;52(2):171-8. doi: 10.1016/0014-2999(78)90203-0.
The ionophore A23187 initiated contractions in both dog coronary artery and rabbit aortic strips in a dose-dependent manner whereas X537A contracted rabbit aortic strips and relaxed KCl-induced contractions in dog coronary artery. Diphenylhydantoin (DPH) and verapamil ccompletely abolished KCl-induced responses in both vascular tissues. DPH (10(-4) M) partially prevented A23187-induced responses in both tissues and verapamil (33 micrometer) partially prevented A23187-induced responses in dog coronary artery but not in rabbit aorta. Phenoxybenzamine (10(-5) M), but not practolol, significantly reduced X537A-induced contractions in rabbit aortic strips but did not affect A23187-induced contractions in either tissue. The inability of DPH and verapamil to completely block the A23187 contractions leads one to conclude that these agents do not completely block calcium influx, or that A23187 does not work solely by increasing the permeability of the cell membrane to calcium. The effect of X537A on rabbit aorta, however, may be mediated at least partially, via release of catecholamines.
离子载体A23187可使犬冠状动脉和兔主动脉条带呈剂量依赖性收缩，而X537A可使兔主动脉条带收缩，并使犬冠状动脉中氯化钾诱导的收缩舒张。苯妥英钠（DPH）和维拉帕米可完全消除两种血管组织中氯化钾诱导的反应。DPH（10⁻⁴ M）部分抑制两种组织中A23187诱导的反应，维拉帕米（33微摩尔）部分抑制犬冠状动脉中A23187诱导的反应，但对兔主动脉无此作用。酚苄明（10⁻⁵ M）而非心得宁可显著降低X537A诱导的兔主动脉条带收缩，但不影响两种组织中A23187诱导的收缩。DPH和维拉帕米无法完全阻断A23187诱导的收缩，这使人们得出结论：这些药物不能完全阻断钙内流，或者A23187并非仅通过增加细胞膜对钙的通透性起作用。然而，X537A对兔主动脉的作用可能至少部分是通过儿茶酚胺的释放介导的。
