Facilitation of L-type Ca2+ currents by fluid flow in rabbit cerebral artery myocytes
Facilitation of L-type Ca2+ currents by fluid flow in rabbit cerebral artery myocytes
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DOI：
10.1254/jphs.fp0050387
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发表时间：
2005-08-01
影响因子：
3.5
通讯作者：
Nakayama, K
中科院分区：
文献类型：
--
作者：
Amano, S;Ishikawa, T;Nakayama, K
血管接受血液动力学力，如血压和流量，这导致肌源性反应。本研究旨在探讨机械应力对兔脑动脉心肌细胞L型电压依赖性钙通道的影响。暴露于16%低渗溶液引起的细胞肿胀增加全细胞Ba 2+电流（I-Ba）的峰值。同样，浴灌注率的升高增加了I-Ba的峰值。然而，通过持续的流体流动刺激降低了响应，并且电流幅度几乎恢复到基线。这种减少的电流被废除的预处理与毒胡萝卜素，这意味着从肌浆网的响应的Ca 2+释放的贡献。这些结果表明，L-型Ca ~（2+）电流的促进不仅由细胞肿胀，但也由脑动脉心肌细胞的液体流动。
Blood vessels are receptive to hemodynamic forces, such as blood pressure and flow, which result in myogenic responses. The present study aimed to investigate the effect of mechanical stresses on L-type voltage-dependent Ca2+ channels in rabbit cerebral artery myocytes. Cell swelling induced by the exposure to a 16% hypotonic solution increased peak values of whole-cell Ba2+ currents (I-Ba). Similarly, an elevation of bath perfusion rate increased peak values Of I-Ba. However, the response was reduced by the continued fluid flow stimulation and the current amplitude almost returned to the baseline. This reduction of the current was abolished by pretreatment with thapsigargin, implying the contribution of Ca2+ release from the sarcoplasmic reticulum to the response. These results suggest that L-type Ca2+ currents are facilitated not only by cell swelling but also by fluid flow in cerebral artery myocytes.