Koller A, Rubányi G, Ligeti L, Kovách A G
Acta Physiol Acad Sci Hung. 1982;59(3):287-90.
Ni-induced coronary vasoconstriction has been studied in the dog heart in situ in the presence of the selective Ca-antagonist verapamil, and after blocking the alpha-receptors with phenoxybenzamine (PBZ). Verapamil totally abolished the coronary blood flow (CBF) and basal conductance (BC) decreasing effect of low doses of Ni2+ (0.02-0.2 mg/kg-1). The effect of higher doses of Ni2+ (2.0-20.0 mg/kg-1) was reversed by verapamil, i.e. high doses of exogenous NiCl2 increased CBF and BC in the presence of verapamil. The CBF decreasing effect of nickel was not significantly influenced by PBZ pretreatment. The results indicate that trace amounts of exogenous NiCl2 induce coronary vasoconstriction in the dog heart in situ by enhancing Ca2+-influx into vascular smooth muscle cells, which is not mediated by alpha-receptors.
在选择性钙拮抗剂维拉帕米存在的情况下，以及在用苯氧苄胺（PBZ）阻断α受体后，对犬心脏原位镍诱导的冠状动脉收缩进行了研究。维拉帕米完全消除了低剂量镍离子（0.02 - 0.2 mg/kg⁻¹）对冠状动脉血流量（CBF）和基础电导（BC）的降低作用。维拉帕米逆转了高剂量镍离子（2.0 - 20.0 mg/kg⁻¹）的作用，即在维拉帕米存在的情况下，高剂量的外源性氯化镍增加了CBF和BC。PBZ预处理对镍降低CBF的作用没有显著影响。结果表明，微量的外源性氯化镍通过增强钙离子流入血管平滑肌细胞，在犬心脏原位诱导冠状动脉收缩，这不是由α受体介导的。
