Randriamampita C, Bismuth G, Debré P, Trautmann A
Laboratoire de Neurobiologie, Ecole Normale Supérieure, Paris, France.
Cell Calcium. 1991 Apr;12(4):313-23. doi: 10.1016/0143-4160(91)90005-y.
An increase in intracellular calcium concentration stimulated by anti-CD2 or CD3 antibodies has been measured with Fura-2 in P28 cells, a human CD4+ T cell clone. This intracellular calcium increase was sensitive to membrane potential changes, being increased when the cells were hyperpolarized and decreased when they were depolarized. The intracellular calcium increase was inhibited by nitrendipine (1-50 microM). Nitrendipine also induced a depolarization of the cells, due to the blockade of a potassium conductance. The inhibition of the calcium increase caused by nitrendipine could be partially reversed by hyperpolarizing the cells with valinomycin. It is concluded that the effects of nitrendipine on potassium channels may account for a large part of the inhibition that nitrendipine exerts on the calcium increase elicited by CD2 or CD3 stimulation.
在人CD4 + T细胞克隆P28细胞中，已用Fura - 2测量了抗CD2或CD3抗体刺激引起的细胞内钙浓度增加。这种细胞内钙增加对膜电位变化敏感，当细胞超极化时增加，去极化时减少。尼群地平（1 - 50微摩尔）可抑制细胞内钙增加。由于钾电导的阻断，尼群地平还诱导细胞去极化。用缬氨霉素使细胞超极化可部分逆转尼群地平引起的钙增加抑制作用。结论是，尼群地平对钾通道的作用可能是其对CD2或CD3刺激引起的钙增加所产生抑制作用的很大一部分原因。
