镍通过强直性Ca2+激活机制诱导离体犬冠状动脉血管收缩。

G Rubányi, L Kalabay, T Pataki, K Hajdú
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引用次数: 0

摘要

低浓度(1微米)氯化镍(NiCl2)诱导离体犬冠状动脉条带的等长力发展。Ni2+的作用线性依赖于细胞外Ca2+浓度在0 - 5.0 mM范围内。维拉帕米(10(-6)- 10(-3)M)不能阻止或消除Ni2+诱导的冠状动脉收缩,但硝普钠即使在低浓度(10(-8)M)下也能拮抗强直力的发展。结果表明,微量NiCl2对离体犬冠状动脉条带力发展的刺激依赖于Ca2+激活t系统介导的跨膜Ca2+内流。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nickel induces vasoconstriction in the isolated canine coronary artery by a tonic Ca2+-activation mechanism.

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.

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