Bakos M, Rubányi G
Acta Physiol Acad Sci Hung. 1982;59(2):175-80.
The coronary vascular effect of various divalent cations and of sodium-metavanadate was compared in isolated perfused rat hearts. Their order of activity was as follows (the concentrations (microM) evoking a half-maximum increase of coronary resistance are indicated (in parentheses): Ni2+ (0.03) greater than Co2+ (0.1) greater than Hg2+ (0.16) greater than VO-3 (0.2) greater than Cu2+ (15) greater than Zn (50). Iron (Fe2+) and cadmium (Cd2+) were ineffective. The order of coronary vasoconstrictor potency of these metal ions differs from the order of their other physico-chemical properties indicating that their coronary action cannot be explained as being singly a consequence of ion-membrane interaction. In contrast to Ni2+, the effect of Hg2+ was totally inhibited by phenoxybenzamine (10(-5)M) indicating that coronary vasoconstriction induced by mercury ions is mediated by alpha-receptors. Coronary vasoconstriction induced by sodium-meta-vanadate was resistant to verapamil while removal of external Ca2+ potentiated its effect. These data suggest that in contrast to Ni2+ and Hg2+, vanadate increases coronary resistance by mobilizing intracellular Ca2+ in vascular smooth muscle cells.
在离体灌注大鼠心脏中比较了各种二价阳离子和偏钒酸钠的冠状血管效应。它们的活性顺序如下（括号内为引起冠状阻力增加一半时的浓度（微摩尔））：Ni2+（0.03）＞Co2+（0.1）＞Hg2+（0.16）＞VO-3（0.2）＞Cu2+（15）＞Zn（50）。铁（Fe2+）和镉（Cd2+）无作用。这些金属离子的冠状血管收缩效力顺序与其其他物理化学性质顺序不同，这表明它们的冠状作用不能单纯解释为离子-膜相互作用的结果。与Ni2+不同，Hg2+的作用完全被酚苄明（10^(-5)M）抑制，这表明汞离子诱导的冠状血管收缩是由α受体介导的。偏钒酸钠诱导的冠状血管收缩对维拉帕米有抗性，而去除细胞外Ca2+可增强其作用。这些数据表明，与Ni2+和Hg2+不同，钒酸盐通过动员血管平滑肌细胞内的Ca2+来增加冠状阻力。
