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目的:确定12-LOX/12-HETE通路是否参与了缺氧抑制Kv通道。方法 :本试验通过血管环技术在细胞水平上观察在12-LO阻断剂CDC和NDGA作用下,缺氧对K+通道的影响,并观察12-HETE对Kv通道的作用是否具有特异性。结果 :我们发现抑制了12-LOX的生成,同时苯肾上腺素引起的在缺氧条件下的肺动脉收缩也被抑制。在常氧和缺氧的条件下,12-LOX被阻断同时也能引起电压门控性K(IKV)通道电流的增加。结论 :上述结果表明,12-HETE能使IKV电流受到抑制能够抑制肺动脉血管的张力,证明内源性12-HETE介导了缺氧对Kv通道的抑制作用。
OBJECTIVE: To determine whether the 12-LOX / 12-HETE pathway is involved in the hypoxic inhibition of Kv channels. Methods: The effects of hypoxia on K + channels were observed by the vascular ring technique at the cellular level under the action of 12-LO blockers CDC and NDGA, and whether the effect of 12-HETE on Kv channel was specific or not was observed. RESULTS: We found that the inhibition of 12-LOX production, and phenylephrine-induced pulmonary artery contraction under hypoxic conditions were also inhibited. Under normoxia and hypoxia conditions, 12-LOX is blocked while also inducing an increase in voltage-gated K (IKV) channel currents. CONCLUSIONS: The above results indicate that inhibition of IKV current by 12-HETE can inhibit pulmonary artery tension and demonstrate that endogenous 12-HETE mediates the inhibitory effect of hypoxia on Kv channels.