Kobayashi S, Kanaide H, Hasegawa M, Yamamoto H, Nakamura M
Br J Exp Pathol. 1985 Dec;66(6):719-28.
We investigated the effects of Ca2+-repletion following depletion on cultured vascular smooth muscle cells (SMCs) from the rat aorta. With Ca2+-repletion, the cells in primary cultures contracted, as indicated by a decrease in cell area. The process was slow (30 min to maximum effect) and reversible (relaxation completed by 120 min). Contraction during Ca2+-repletion was never observed in subcultured cells. The SMCs in primary culture after treatment maintained the ability to grow and to exclude dye, with a normal plating efficiency. There was no treatment-related additional leakage of intracellular enzymes, LDH and CPK, into the medium. Ca2+-repletion at first accelerated the 45Ca uptake by SMCs (1-5 min after repletion) and then increased Ca2+ efflux after about 10 min of Ca2+-repletion. We conclude that Ca2+-repletion after depletion induces a transient and reversible contraction of vascular SMCs in primary culture, without cell injury and in association with a transient increase in Ca2+ influx and then efflux. This phenomenon may relate to the decrease in perfusion flow in hearts and kidneys during Ca2+-repletion after depletion (Ca2+-paradox).
我们研究了钙耗竭后再补充钙对大鼠主动脉培养血管平滑肌细胞（SMCs）的影响。随着钙的再补充，原代培养的细胞发生收缩，表现为细胞面积减小。该过程缓慢（30分钟达到最大效应）且可逆（120分钟内完成舒张）。传代培养的细胞在钙再补充过程中从未观察到收缩现象。原代培养经处理后的平滑肌细胞保持生长和排斥染料的能力，接种效率正常。未观察到与处理相关的细胞内酶（乳酸脱氢酶和肌酸磷酸激酶）额外泄漏到培养基中。钙再补充最初加速了平滑肌细胞对45Ca的摄取（再补充后1 - 5分钟），然后在钙再补充约10分钟后增加了钙外流。我们得出结论，钙耗竭后再补充钙可诱导原代培养的血管平滑肌细胞发生短暂且可逆的收缩，无细胞损伤，且与钙内流短暂增加随后外流有关。这种现象可能与钙耗竭后再补充钙（钙反常）期间心脏和肾脏灌注流量减少有关。
