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首页> 外文期刊>Life sciences >Effects of Cl- channel blockers on endothelin-1-induced proliferation of rat vascular smooth muscle cells.
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Effects of Cl- channel blockers on endothelin-1-induced proliferation of rat vascular smooth muscle cells.

机译：Cl-通道阻滞剂对内皮素-1诱导的大鼠血管平滑肌细胞增殖的影响。

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摘要

The effects of Cl- channel blockers on endothelin-1 (ET-1)-induced proliferation of rat aortic vascular smooth muscle cells (VSMC) were examined. We found ET-1 concentration-dependently increased cell count and [3H]-thymidine incorporation into VSMC, with EC50 values of 24.8 and 11.4 nM, respectively. Both nifedipine and SK&F96365 inhibited 10 nM ET-1-induced [3H]-thymidine incorporation into VSMC with the maximal inhibitory concentrations of 1 and 10 microM, respectively. DIDS inhibited 10 nM ET-1-induced increase in cell count and [3H]-thymidine incorporation into VSMC in a concentration-dependent manner, whereas other Cl- channel blockers including IAA-94, NPPB, DPC, SITS and furosemide did not produce these effects. 3 microM DIDS reduced 10 nM ET-1-induced sustained increase in cytoplasmic Ca2+ concentration ([Ca2+]) by 52%. Pretreatment of VSMC with 1 microM nifedipine completely inhibited the DIDS effect on 10 nM ET-1-induced [3H]-thymidine incorporation into VSMC and sustained increase in [Ca2+]i, whereas pretreatment with 10 microM SK&F96365 did not completely block these effects of DIDS. DIDS did not affect ET-1-induced Ca2+ release and 30 mM KCl-induced increase in [Ca2+]i. Our data suggest that DIDS-sensitive Cl- channels mediate VSMC proliferation induced by ET-1 by mechanisms related to membrane depolarization and Ca2+ influx through voltage-dependent Ca2+ channels.
机译：检查了Cl-通道阻滞剂对内皮素-1（ET-1）诱导的大鼠主动脉血管平滑肌细胞（VSMC）增殖的影响。我们发现ET-1浓度依赖性地增加细胞计数和[3H]-胸苷掺入VSMC，EC50值分别为24.8和11.4 nM。硝苯地平和SK＆F96365均以最大抑制浓度分别为1和10 microM抑制10 nM ET-1诱导的[3H]-胸苷掺入VSMC。 DIDS以浓度依赖的方式抑制了10 nM ET-1诱导的细胞计数增加和[3H]-胸苷掺入VSMC，而其他Cl-通道阻滞剂，包括IAA-94，NPPB，DPC，SITS和呋塞米则未产生这些影响。 3 microM DIDS使10 nM ET-1诱导的细胞质Ca2 +浓度（[Ca2 +]）持续增加降低了52％。用1 microM硝苯地平预处理VSMC可以完全抑制DIDS对10 nM ET-1诱导的[3H]-胸腺嘧啶核苷掺入VSMC中的作用，并持续增加[Ca2 +] i，而用10 microM SK＆F96365预处理则不能完全阻断DIDS。 DIDS不影响ET-1诱导的Ca2 +释放和30 mM KCl诱导的[Ca2 +] i增加。我们的数据表明，DIDS敏感的Cl-通道通过与膜去极化和Ca2 +通过电压依赖性Ca2 +通道流入有关的机制介导ET-1诱导的VSMC增殖。

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