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内皮素-1诱导大鼠尾动脉收缩的钙离子依赖性

Ca2(+)-dependence of endothelin-1 induced contraction of rat tail artery.

作者信息

Huang X N, Takayanagi I, Kurata R, Hisayama T

机构信息

Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences, Chiba, Japan.

出版信息

Gen Pharmacol. 1991;22(2):399-402. doi: 10.1016/0306-3623(91)90471-h.

Abstract
  1. In rat tail artery, endothelin-1(ET-1) caused an increase in the cytosolic free Ca2+ level ([Ca2+]i) followed by a relatively sustained but not steady-state contraction in Ca2+ containing solution. 2. In the early phase of the contraction, the rate of increase in [Ca2+]i, was much faster than that in muscle tension. However, after the increases in [Ca2+]i and muscle tension reached at their peaks, there was a good correlation between the changes of the two parameters. 3. ET-1 could not induce an apparent contractile response in Ca2(+)-free medium, notwithstanding it evoked a [Ca2+]i transient in this medium. 4. The results indicate that ET-1 induce a contraction of rat tail artery which is almost fully dependent on the [Ca2+]i changes, and may inhibit the Ca2(+)-sensitivity of the contractile filaments in the early phase of the contraction.
摘要
  1. 在大鼠尾动脉中,内皮素 -1(ET -1)使胞质游离钙离子水平([Ca2+]i)升高,随后在含钙溶液中引发相对持续但非稳态的收缩。2. 在收缩早期,[Ca2+]i的升高速率比肌肉张力的升高速率快得多。然而,在[Ca2+]i和肌肉张力升高至峰值后,这两个参数的变化之间存在良好的相关性。3. 尽管ET -1在无Ca2+的培养基中引发了[Ca2+]i瞬变,但它在该培养基中不能诱导明显的收缩反应。4. 结果表明,ET -1诱导大鼠尾动脉收缩,这几乎完全依赖于[Ca2+]i的变化,并且在收缩早期可能抑制收缩细丝对Ca2+的敏感性。

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