Niwa A, Suzuki A
J Toxicol Sci. 1982 Feb;7(1):51-60. doi: 10.2131/jts.7.51.
A possible mechanism for the pressor effect of cadmium was investigated in isolated rat thoracic aorta. Cadmium produced contractions at low concentrations, but relaxations at high concentrations. Phentolamine, a sympathetic alpha blocking agent did not inhibit the cadmium-induced contractions. These contractions were reduced in accordance with the decrease in Ca content in medium and were abolished in Ca-free medium, rather inducing a small degree of relaxation. When low concentrations of cadmium were applied repeatedly for a short period of time, the contractions were remarkably reduced and finally abolished. Noradrenaline-induced contractions were not affected after the completion of cadmium-tachyphylaxis. Low concentrations of cadmium potentiated K-, Ba- and noradrenaline-induced contractions, while high concentrations suppressed them. These results suggest that cadmium-induced contractions are dependent on external Ca and that they are produced by direct stimulation on the cell membrane. In addition, low concentrations of cadmium accelerate Ca availability, while high concentrations inhibit it.
在离体大鼠胸主动脉中研究了镉升压作用的一种可能机制。镉在低浓度时引起收缩，但在高浓度时引起舒张。酚妥拉明，一种交感神经α阻滞剂，并不抑制镉诱导的收缩。这些收缩随着培养基中钙含量的降低而减少，并且在无钙培养基中消失，反而诱导了轻微的舒张。当在短时间内反复应用低浓度的镉时，收缩明显减少并最终消失。镉快速耐受完成后，去甲肾上腺素诱导的收缩不受影响。低浓度的镉增强钾、钡和去甲肾上腺素诱导的收缩，而高浓度则抑制它们。这些结果表明，镉诱导的收缩依赖于细胞外钙，并且它们是由对细胞膜的直接刺激产生的。此外，低浓度的镉加速钙的可用性，而高浓度则抑制它。
