氟化物钠诱导的通透性大鼠肠系膜动脉钙敏化。
Calcium sensitization induced by sodium fluoride in permeabilized rat mesenteric arteries.
机构信息
Department of Pharmacology, Kyungpook National University School of Medicine, Daegu 700-422, Korea.
出版信息
Korean J Physiol Pharmacol. 2010 Feb;14(1):51-7. doi: 10.4196/kjpp.2010.14.1.51. Epub 2010 Feb 28.
It was hypothesized that NaF induces calcium sensitization in Ca(2+)-controlled solution in permeabilized rat mesenteric arteries. Rat mesenteric arteries were permeabilized with beta-escin and subjected to tension measurement. NaF potentiated the concentration-response curves to Ca(2+) (decreased EC(50) and increased E(max)). Cumulative addition of NaF (4.0, 8.0 and 16 mM) also increased vascular tension in Ca(2+)-controlled solution at pCa 7.0 or pCa 6.5, but not at pCa 8.0. NaF-induced vasocontraction and GTPgammaS-induced vasocontraction were not additive. NaF-induced vasocontraction at pCa 7.0 was inhibited by pretreatment with Rho kinase inhibitors H1152 or Y27632 but not with a MLCK inhibitor ML-7 or a PKC inhibitor Ro31-8220. NaF induces calcium sensitization in a Ca(2+)-dependent manner in beta-escin-permeabilized rat mesenteric arteries. These results suggest that NaF is an activator of the Rho kinase signaling pathway during vascular contraction.
据推测，NaF 在通透的大鼠肠系膜动脉的钙离子控制溶液中诱导钙敏化。用β-七叶皂甙素通透大鼠肠系膜动脉，并进行张力测量。NaF 增强了钙（EC50 降低，E(max) 增加）反应曲线对 Ca(2+)的浓度反应。在 pCa7.0 或 pCa6.5 时，累积添加 NaF（4.0、8.0 和 16 mM）也会增加 Ca(2+)-控制溶液中的血管张力，但在 pCa8.0 时不会。NaF 诱导的血管收缩和 GTPγS 诱导的血管收缩不是相加的。在 pCa7.0 时，用 Rho 激酶抑制剂 H1152 或 Y27632 预处理可抑制 NaF 诱导的血管收缩，但用肌球蛋白轻链激酶抑制剂 ML-7 或蛋白激酶 C 抑制剂 Ro31-8220 则不能。NaF 以钙离子依赖的方式在β-七叶皂甙素通透的大鼠肠系膜动脉中诱导钙敏化。这些结果表明，在血管收缩期间，NaF 是 Rho 激酶信号通路的激活剂。
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