Kv7通道對(duì)人胎盤絨毛膜板動(dòng)脈血管環(huán)舒縮功能的影響及其機(jī)制
發(fā)布時(shí)間：2018-10-18 10:58
【摘要】：目的探討Kv7通道對(duì)人胎盤絨毛膜板動(dòng)脈(CPAs)血管環(huán)舒縮功能的影響及其可能的機(jī)制。方法取內(nèi)皮完整或去內(nèi)皮CPAs血管環(huán),分別加入累積濃度遞增的XE991、Linopirdine或二甲基亞砜(DMSO),計(jì)算收縮率。取去內(nèi)皮CPAs血管環(huán),經(jīng)過(guò)或者不經(jīng)過(guò)XE991孵育后加入累積濃度遞增的U46619,計(jì)算收縮率。將去內(nèi)皮CPAs血管環(huán)加入1×10~(-7)mol/L U46619進(jìn)行預(yù)收縮處理,分別加入累積濃度遞增的Kv7通道開放劑[Acrylamide(S)-1、Retigabine、BMS-204352、ML277]及DMSO,計(jì)算舒張率。取去內(nèi)皮CPAs血管環(huán),分別經(jīng)硝苯地平、levcromakalim及無(wú)鈣液處理后加入XE991(1×10~(-5)mol/L)或Linopirdine(1×10-4mol/L),計(jì)算處理前后收縮率。結(jié)果內(nèi)皮完整CPAs血管環(huán)與去內(nèi)皮CPAs血管環(huán)收縮率隨著XE991、Linopirdine濃度的升高而升高,分別于5×10~(-5)、1×10~(-4)mol/L時(shí)收縮率最大。與加入同濃度DMSO作用后比較,內(nèi)皮完整CPAs血管環(huán)與去內(nèi)皮CPAs血管環(huán)加入XE991或Linopirdine作用后的收縮率均升高(P均0.01)。內(nèi)皮完整CPAs血管環(huán)與去內(nèi)皮CPAs血管環(huán)加入同濃度XE991或Linopirdine作用后的收縮率比較差異均無(wú)統(tǒng)計(jì)學(xué)意義(P均0.05)。隨著U46619濃度的升高,經(jīng)過(guò)或者不經(jīng)過(guò)XE991孵育的去內(nèi)皮CPAs血管環(huán)收縮率均逐漸升高,但經(jīng)過(guò)孵育后升高更明顯(P均0.01)。U46619預(yù)收縮CPAs血管環(huán)加入1×10~(-4)mol/L Acrylamide(S)-1、Retigabine、BMS-204352作用后的舒張率均高于加入同濃度DMSO(P均0.01),加入ML277作用后的舒張率無(wú)明顯變化(P均0.05)。XE991組和Linopirdine組經(jīng)硝苯地平、levcromakalim及無(wú)鈣臺(tái)式液處理后的收縮率均低于處理前(P均0.01)。結(jié)論 Kv7通道通過(guò)介導(dǎo)細(xì)胞膜靜息K+電導(dǎo)和靜息膜電位的改變而參與調(diào)節(jié)CPAs血管環(huán)的舒縮;阻斷Kv7通道可引起CPAs平滑肌細(xì)胞去極化,激活L型鈣離子通道,引起Ca2+內(nèi)流和血管收縮。
[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.
【作者單位】： 西南醫(yī)科大學(xué)附屬醫(yī)院;
【基金】：四川省科學(xué)技術(shù)廳與瀘州市人民政府、瀘州醫(yī)學(xué)院聯(lián)合科研專項(xiàng)資金計(jì)劃項(xiàng)目(川科發(fā)計(jì)[2014]10號(hào))
【分類號(hào)】：R714.5
本文編號(hào)：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.
【作者單位】： 西南醫(yī)科大學(xué)附屬醫(yī)院;
【基金】：四川省科學(xué)技術(shù)廳與瀘州市人民政府、瀘州醫(yī)學(xué)院聯(lián)合科研專項(xiàng)資金計(jì)劃項(xiàng)目(川科發(fā)計(jì)[2014]10號(hào))
【分類號(hào)】：R714.5
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