Knot H J, de Ree M M, Gähwiler B H, Rüegg U T
Sandoz Pharma Ltd., Basel, Switzerland.
J Cardiovasc Pharmacol. 1991;18 Suppl 10:S7-14.
The A7r5 smooth muscle cell line, which originally was derived from fetal rat aorta, shows spontaneous calcium oscillations associated with electrical activity (frequency of 0.2-0.5 Hz). Organic calcium antagonists such as isradipine (10(-8) M) stopped the calcium oscillations whereas calcium agonists (e.g., Bay K 8644, 10(-8) M) increased the frequency and amplitude of calcium oscillations without changing the shape of the electrical spikes. The enantiomers of the dihydropyridine SDZ 202-791 known to have opposite activity with respect to L-type Ca2+ channels antagonized each other when tested for their effects on the calcium oscillations. The modulation of the activity of these cells by inorganic ions that affect Ca2+ and K+ channels was also investigated. The addition of barium chloride (10(-4) M) to the bathing solution increased the spiking rate whereas cadmium chloride (10(-6) M) abolished the spikes. The vasoconstrictor peptide vasopressin first induced a hyperpolarization associated with the cessation of spiking activity followed by a slow depolarization. The intracellular Ca2+ concentration ([Ca2+]i), measured with the calcium indicator fura-2, was increased transiently to a level about 10-fold above basal and then gained a new steady state at about twice the basal level. Vasopressin stimulated Ca2+ release from intracellular stores (via InsP3), resulting in membrane hyperpolarization through activation of Ca(2+)-activated K+ channels. The late and long-lasting [Ca2+]i elevation was due to Ca2+ influx through dihydropyridine-insensitive channels.(ABSTRACT TRUNCATED AT 250 WORDS)
A7r5平滑肌细胞系最初源自胎鼠主动脉，表现出与电活动相关的自发钙振荡（频率为0.2 - 0.5赫兹）。有机钙拮抗剂如伊拉地平（10⁻⁸M）可使钙振荡停止，而钙激动剂（如Bay K 8644，10⁻⁸M）可增加钙振荡的频率和幅度，且不改变电尖峰的形状。已知对L型Ca²⁺通道具有相反活性的二氢吡啶SDZ 202 - 791的对映体在测试其对钙振荡的影响时相互拮抗。还研究了影响Ca²⁺和K⁺通道的无机离子对这些细胞活性的调节作用。向浴液中添加氯化钡（10⁻⁴M）可提高放电率，而氯化镉（10⁻⁶M）可消除尖峰。血管收缩肽血管加压素首先诱导与放电活动停止相关的超极化，随后是缓慢的去极化。用钙指示剂fura - 2测量的细胞内Ca²⁺浓度（[Ca²⁺]i）短暂升高至比基础水平高约10倍的水平，然后在约为基础水平两倍的水平达到新的稳态。血管加压素刺激细胞内钙库释放Ca²⁺（通过InsP3），通过激活Ca²⁺激活的K⁺通道导致膜超极化。后期持久的[Ca²⁺]i升高是由于Ca²⁺通过对二氢吡啶不敏感的通道内流。（摘要截断于250字）
