Rubányi G, Kalabay L, Pataki T, Hajdú K
Acta Physiol Acad Sci Hung. 1982;59(2):155-9.
Nickel chloride (NiCl2) at low concentration (1 microM) induced isometric force development in isolated canine coronary artery strips. The Ni2+-action was linearly dependent on extracellular Ca2+-concentration in the range of 0 to 5.0 mM. Verapamil (10(-6) - 10(-3) M) did not prevent or abolish Ni2+-induced coronary contraction, but nitroprusside sodium even at low concentration (10(-8) M) antagonized the tonic force development. The results indicate that the stimulation of force development by trace amounts of NiCl2 in isolated canine coronary artery strips is dependent on transmembrane Ca2+-influx which is mediated by the T-system of Ca2+-activation.
低浓度（1微摩尔）的氯化镍（NiCl₂）可诱导离体犬冠状动脉条产生等长力。在0至5.0毫摩尔范围内，Ni²⁺的作用与细胞外Ca²⁺浓度呈线性相关。维拉帕米（10⁻⁶ - 10⁻³摩尔/升）不能预防或消除Ni²⁺诱导的冠状动脉收缩，但硝普钠即使在低浓度（10⁻⁸摩尔/升）时也能拮抗张力的产生。结果表明，微量NiCl₂刺激离体犬冠状动脉条产生力的过程依赖于跨膜Ca²⁺内流，该内流由Ca²⁺激活的T系统介导。
