Kv7通道对人胎盘绒毛膜板动脉血管环舒缩功能的影响及其机制
发布时间：2018-10-18 10:58
【摘要】：目的探讨Kv7通道对人胎盘绒毛膜板动脉(CPAs)血管环舒缩功能的影响及其可能的机制。方法取内皮完整或去内皮CPAs血管环,分别加入累积浓度递增的XE991、Linopirdine或二甲基亚砜(DMSO),计算收缩率。取去内皮CPAs血管环,经过或者不经过XE991孵育后加入累积浓度递增的U46619,计算收缩率。将去内皮CPAs血管环加入1×10~(-7)mol/L U46619进行预收缩处理,分别加入累积浓度递增的Kv7通道开放剂[Acrylamide(S)-1、Retigabine、BMS-204352、ML277]及DMSO,计算舒张率。取去内皮CPAs血管环,分别经硝苯地平、levcromakalim及无钙液处理后加入XE991(1×10~(-5)mol/L)或Linopirdine(1×10-4mol/L),计算处理前后收缩率。结果内皮完整CPAs血管环与去内皮CPAs血管环收缩率随着XE991、Linopirdine浓度的升高而升高,分别于5×10~(-5)、1×10~(-4)mol/L时收缩率最大。与加入同浓度DMSO作用后比较,内皮完整CPAs血管环与去内皮CPAs血管环加入XE991或Linopirdine作用后的收缩率均升高(P均0.01)。内皮完整CPAs血管环与去内皮CPAs血管环加入同浓度XE991或Linopirdine作用后的收缩率比较差异均无统计学意义(P均0.05)。随着U46619浓度的升高,经过或者不经过XE991孵育的去内皮CPAs血管环收缩率均逐渐升高,但经过孵育后升高更明显(P均0.01)。U46619预收缩CPAs血管环加入1×10~(-4)mol/L Acrylamide(S)-1、Retigabine、BMS-204352作用后的舒张率均高于加入同浓度DMSO(P均0.01),加入ML277作用后的舒张率无明显变化(P均0.05)。XE991组和Linopirdine组经硝苯地平、levcromakalim及无钙台式液处理后的收缩率均低于处理前(P均0.01)。结论 Kv7通道通过介导细胞膜静息K+电导和静息膜电位的改变而参与调节CPAs血管环的舒缩;阻断Kv7通道可引起CPAs平滑肌细胞去极化,激活L型钙离子通道,引起Ca2+内流和血管收缩。
[Abstract]:Objective to investigate the effect of Kv7 channel on the vasomotor function of human placental chorionic lamellar artery (CPAs) and its possible mechanism. Methods Endothelial intact or deendothelified CPAs rings were added to the cumulative concentration of XE991,Linopirdine or dimethyl sulfoxide (DMSO), to calculate the contraction rate. The endothelial CPAs rings were removed and the cumulative concentration of U46619 was added after or without XE991 incubation to calculate the contraction rate. Endothelial CPAs rings were added to 1 脳 10 ~ (-7) mol/L U46619 for pre-contraction, and Kv7 channel openers with increasing cumulative concentration were added respectively [Acrylamide (S) -1 Retigabine BMS-204352 ML277] and DMSO, to calculate the diastolic rate. The endothelial CPAs rings were removed and treated with nifedipine, levcromakalim and calcium free solution, then XE991 (1 脳 10 ~ (-5) mol/L) or Linopirdine (1 脳 10-4mol/L) were added to calculate the contraction rate before and after treatment. Results the contractile rate of intact and deendothelified CPAs rings increased with the increase of XE991,Linopirdine concentration, which was the highest at 5 脳 10 ~ (-5) mol/L and 1 脳 10 ~ (-4) mol/L, respectively. Compared with the same concentration of DMSO, the contractile rate of the endothelial intact CPAs rings and the deendothelified CPAs rings increased after the addition of XE991 or Linopirdine (P0.01, respectively). There was no significant difference in the contractile rate between the endothelial intact CPAs vascular ring and the deendothelified CPAs vascular ring after the addition of the same concentration of XE991 or Linopirdine (P 0.05). With the increase of U46619 concentration, the constriction rate of endothelium-free CPAs rings increased with or without XE991 incubation. But after incubation, the diastolic rate of U46619 precontracted CPAs rings was higher than that of DMSO (P at the same concentration after adding 1 脳 10 ~ (-4) mol/L Acrylamide (S) ~ (-1) Retigabine BMS-204352 (P0. 01). The diastolic rate of XE991 group and Linopirdine group was not significantly changed after adding ML277 (all P 0. 05). The vasodilation rate of U46619 precontracted CPAs annulus was higher than that of ML277 after adding 1 脳 10 ~ (-4) mol/L Acrylamide (S)-1 ~ (-1) Retigabine BMS-204352 (all P 0. 05). The contraction rate of levcromakalim and calcium-free tabletop solution was lower than that before treatment (P 0.01). Conclusion Kv7 channels mediate the changes of resting K conductance and resting membrane potential to regulate the contraction and relaxation of CPAs vascular rings, and blocking Kv7 channels can induce the depolarization of CPAs smooth muscle cells and activate L-type calcium channels. Causes Ca2 inflow and vasoconstriction.
【作者单位】： 西南医科大学附属医院;
【基金】：四川省科学技术厅与泸州市人民政府、泸州医学院联合科研专项资金计划项目(川科发计[2014]10号)
【分类号】：R714.5
本文编号：2278913
[Abstract]:Objective to investigate the effect of Kv7 channel on the vasomotor function of human placental chorionic lamellar artery (CPAs) and its possible mechanism. Methods Endothelial intact or deendothelified CPAs rings were added to the cumulative concentration of XE991,Linopirdine or dimethyl sulfoxide (DMSO), to calculate the contraction rate. The endothelial CPAs rings were removed and the cumulative concentration of U46619 was added after or without XE991 incubation to calculate the contraction rate. Endothelial CPAs rings were added to 1 脳 10 ~ (-7) mol/L U46619 for pre-contraction, and Kv7 channel openers with increasing cumulative concentration were added respectively [Acrylamide (S) -1 Retigabine BMS-204352 ML277] and DMSO, to calculate the diastolic rate. The endothelial CPAs rings were removed and treated with nifedipine, levcromakalim and calcium free solution, then XE991 (1 脳 10 ~ (-5) mol/L) or Linopirdine (1 脳 10-4mol/L) were added to calculate the contraction rate before and after treatment. Results the contractile rate of intact and deendothelified CPAs rings increased with the increase of XE991,Linopirdine concentration, which was the highest at 5 脳 10 ~ (-5) mol/L and 1 脳 10 ~ (-4) mol/L, respectively. Compared with the same concentration of DMSO, the contractile rate of the endothelial intact CPAs rings and the deendothelified CPAs rings increased after the addition of XE991 or Linopirdine (P0.01, respectively). There was no significant difference in the contractile rate between the endothelial intact CPAs vascular ring and the deendothelified CPAs vascular ring after the addition of the same concentration of XE991 or Linopirdine (P 0.05). With the increase of U46619 concentration, the constriction rate of endothelium-free CPAs rings increased with or without XE991 incubation. But after incubation, the diastolic rate of U46619 precontracted CPAs rings was higher than that of DMSO (P at the same concentration after adding 1 脳 10 ~ (-4) mol/L Acrylamide (S) ~ (-1) Retigabine BMS-204352 (P0. 01). The diastolic rate of XE991 group and Linopirdine group was not significantly changed after adding ML277 (all P 0. 05). The vasodilation rate of U46619 precontracted CPAs annulus was higher than that of ML277 after adding 1 脳 10 ~ (-4) mol/L Acrylamide (S)-1 ~ (-1) Retigabine BMS-204352 (all P 0. 05). The contraction rate of levcromakalim and calcium-free tabletop solution was lower than that before treatment (P 0.01). Conclusion Kv7 channels mediate the changes of resting K conductance and resting membrane potential to regulate the contraction and relaxation of CPAs vascular rings, and blocking Kv7 channels can induce the depolarization of CPAs smooth muscle cells and activate L-type calcium channels. Causes Ca2 inflow and vasoconstriction.
【作者单位】： 西南医科大学附属医院;
【基金】：四川省科学技术厅与泸州市人民政府、泸州医学院联合科研专项资金计划项目(川科发计[2014]10号)
【分类号】：R714.5
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