Sawamura M, Kobayashi Y, Nara Y, Hattori K, Yamori Y
Biochem Biophys Res Commun. 1987 May 29;145(1):494-501. doi: 10.1016/0006-291x(87)91348-9.
In rat thoracic aorta, 12-0-tetradecanoyl-phorbol-13-acetate (TPA) caused a slowly onset, sustained vascular contraction. The contraction was markedly reduced in the absence of extracellular Ca2+, although small tension development was still observed. The tension developed by TPA in the presence of Ca2+ was decreased by serial addition of a Ca2+-channel blocker, verapamil in a concentration-dependent manner. TPA could cause vascular contraction to almost maximum level at lower concentration of extracellular Ca2+, compared with KCl- or norepinephrine-induced contraction. These results suggest that extracellular Ca2+ which influxes through Ca2+-channels into cytoplasm is necessary for full tension development by TPA, and that TPA increases sensitivity of contractile mechanisms coupling with Ca2+.
在大鼠胸主动脉中,12-0-十四烷酰佛波醇-13-乙酸酯(TPA)引起缓慢起效的持续性血管收缩。在无细胞外Ca2+时,收缩明显减弱,尽管仍观察到少量张力产生。在有Ca2+存在时,TPA产生的张力随Ca2+通道阻滞剂维拉帕米的逐次添加而以浓度依赖方式降低。与氯化钾或去甲肾上腺素诱导的收缩相比,TPA在较低细胞外Ca2+浓度下可使血管收缩达到几乎最大水平。这些结果表明,通过Ca2+通道流入细胞质的细胞外Ca2+是TPA产生完全张力所必需的,并且TPA增加了与Ca2+偶联的收缩机制的敏感性。