Mechanism of barium‐induced contraction in the vascular smooth muscle of rabbit aorta
Mechanism of barium‐induced contraction in the vascular smooth muscle of rabbit aorta
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DOI：
10.1111/j.1476-5381.1986.tb16255.x
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发表时间：
1986-08
影响因子：
7.3
通讯作者：
H. Karaki;N. Satake;S. Shibata
中科院分区：
文献类型：
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作者：
H. Karaki;N. Satake;S. Shibata
1在含有1.5 mm Ca 2+的溶液中，累积应用0.3 - 10.0 mm Ba 2+诱导兔主动脉的浓度依赖性收缩。钙通道抑制剂维拉帕米（10−6 m）、硝苯地平（10−7 m）和镧（2.0 mm）可降低这种收缩，钙通道促进剂Bay K 8644（10−7 m）可增强这种收缩。2在含有EGTA（1.0 mm）的无钙溶液中，累积应用Ba 2+仍诱导浓度依赖性收缩，其最大收缩张力与存在1.5 mm Ca 2+时相当。3不依赖于外部Ca 2+的Ba 2+诱导的收缩也被维拉帕米、硝苯地平和镧抑制，并被Bay K 8644增强。高浓度（65.4 mM）的K+增强了Ba 2+诱导的收缩，而去甲肾上腺素（10−6 mM）没有这种作用。4为了耗尽细胞中可释放的Ca 2+储存，在无Ca 2+溶液中用去甲肾上腺素（10 - 6 μ m）和/或咖啡因（20.0 μ m）处理肌肉条。在这种Ca 2+耗尽的肌肉中，Ba 2+仍然诱导与没有这种处理的肌肉相似幅度的收缩。此外，在不含Ca 2+的溶液中第二次施加Ba 2+诱导了与第一次施加Ba 2+诱导的收缩相似的收缩。5这些结果表明，Ba 2+使细胞膜去极化并打开电压依赖性Ca 2+通道，导致在Ca 2+存在下的Ca 2+内流。在没有外部Ca 2+的情况下，Ba 2+可以通过电压依赖性Ca 2+通道进入细胞并诱导收缩，而不动员对去甲肾上腺素和咖啡因敏感的Ca 2+库。
1 In a solution containing 1.5 mm Ca2+, cumulative application of 0.3−10.0 mm Ba2+ induced a concentration‐dependent contraction of the rabbit aorta. This contraction was reduced by the Ca2+ channel inhibitors, verapamil (10−6 m), nifedipine (10−7 m) and lanthanum (2.0 mm), and was potentiated by the Ca2+ channel facilitator, Bay K 8644 (10−7 m). 2 In a Ca2+‐free solution containing EGTA (1.0 mm), cumulative application of Ba2+ still induced a concentration‐dependent contraction, the maximum contractile tension of which was comparable to that in the presence of 1.5 mm Ca2+. 3 The Ba2+‐induced contraction which was not dependent on the external Ca2+ was also inhibited by verapamil, nifedipine and lanthanum and was potentiated by Bay K 8644. A high concentration (65.4 mm) of K+ potentiated this Ba2+‐induced contraction whereas noradrenaline (10−6 m) did not have such an effect. 4 In order to deplete the releasable Ca2+ store in the cell, the muscle strip was treated with noradrenaline (10−6 m) and/or caffeine (20.0 mm) in a Ca2+‐free solution. In such a Ca2+‐depleted muscle, Ba2+ still induced a contraction of a similar magnitude to that without such treatment. Further, the second application of Ba2+ in a Ca2+‐free solution induced a similar contraction to that induced by the first application of Ba2+. 5 These results suggest that Ba2+ depolarizes the cell membrane and opens the voltage‐dependent Ca2+ channels resulting in a Ca2+ influx in the presence of Ca2+. In the absence of external Ca2+, Ba2+ may enter the cell through the voltage‐dependent Ca2+ channels and induce contraction without mobilizing the Ca2+ store which is sensitive to noradrenaline and caffeine.