Endothelium‐derived hyperpolarizing factor and potassium use different mechanisms to induce relaxation of human subcutaneous resistance arteries
Endothelium‐derived hyperpolarizing factor and potassium use different mechanisms to induce relaxation of human subcutaneous resistance arteries
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内皮源性超极化因子和钾利用不同机制诱导人体皮下阻力动脉松弛
DOI：
10.1038/sj.bjp.0704143
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发表时间：
2001
影响因子：
7.3
通讯作者：
P. Hadoke
中科院分区：
文献类型：
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作者：
C. McIntyre;C H Buckley;G C Jones;T C Sandeep;R C Andrews;A. I. Elliott;G A Gray;B C Williams;J A McKnight;B R Walker;P. Hadoke
本研究通过比较ACh和KCl在人皮下阻力动脉中产生的舒张反应，检验了K+释放解释EDHF活性的假设。将来自人皮下脂肪活检组织的阻力动脉（内径244±12μm，n=48）悬挂在钢丝肌描记器中。用去甲肾上腺素（NA; 0.1 - 3 μM）收缩后，获得ACh（10−9 - 3×10−5 M）和KCl（2.5 - 25 mM）的累积浓度响应曲线。 ACh（Emax 99.07±9.61%; − LogIC 50 7.03±0.22; n=9）和KCl（Emax 74.14±5.61%; − LogIC 50 2.12±0.07; n=10）诱导的舒张作用通过去除内皮细胞而减弱（P<0.0001）（Emax分别为8.21±5.39%和11.56± 8.49%; n=6 - 7）。 吲哚美辛（10 μM）没有改变ACh诱导的舒张，而L-NOARG（100 μM）降低了这种反应（Emax 61.7± 3.4%，P<0.0001; n=6）。 ChTx（50 nM）和apamin（30 nM）的组合减弱了ACh诱导舒张的L-NOARG不敏感成分（Emax：15.2± 10.5%，P<0.002，n=6），尽管这些动脉保留了响应100 μM SIN-1的舒张能力（Emax 127.6± 13.0%，n=3）。 暴露于BaCl 2（30 μM）和哇巴因（1 mM）不会减弱ACh介导的舒张的L-NOARG抵抗成分（Emax，76.09±8.92，P=0.16; n=5）。 KCl介导的舒张不受L-NOARG+吲哚美辛（Emax; 68.1± 5.6%，P=0.33; n=5）或L-NOARG/吲哚美辛/ChTx/apamin组合（Emax; 86.61± 14.02%，P=0.35; n=6）的影响。相比之下，L-NOARG、吲哚美辛、哇巴因和BaCl 2的组合消除了这种反应（Emax，5.67± 2.59%，P<0.0001，n=6）。KCl介导的舒张特征与ACh反应的一氧化氮/前列腺素非依赖性成分不同，并且是内皮依赖性的，表明K+在人皮下阻力动脉中不作为EDHF。
This investigation examined the hypothesis that release of K+ accounts for EDHF activity by comparing relaxant responses produced by ACh and KCl in human subcutaneous resistance arteries. Resistance arteries (internal diameter 244±12 μm, n=48) from human subcutaneous fat biopsies were suspended in a wire myograph. Cumulative concentration‐response curves were obtained for ACh (10−9 – 3×10−5 M) and KCl (2.5 – 25 mM) following contraction with noradrenaline (NA; 0.1 – 3 μM). ACh (Emax 99.07±9.61%; −LogIC50 7.03±0.22; n=9) and KCl (Emax 74.14±5.61%; −LogIC50 2.12±0.07; n=10)‐induced relaxations were attenuated (P<0.0001) by removal of the endothelium (Emax 8.21±5.39% and 11.56±8.49%, respectively; n=6 – 7). Indomethacin (10 μM) did not alter ACh‐induced relaxation whereas L‐NOARG (100 μM) reduced this response (Emax 61.7±3.4%, P<0.0001; n=6). The combination of ChTx (50 nM) and apamin (30 nM) attenuated the L‐NOARG‐insensitive component of ACh‐induced relaxation (Emax: 15.2±10.5%, P<0.002, n=6) although these arteries retained the ability to relax in response to 100 μM SIN‐1 (Emax 127.6±13.0%, n=3). Exposure to BaCl2 (30 μM) and Ouabain (1 mM) did not attenuate the L‐NOARG resistant component of ACh‐mediated relaxation (Emax, 76.09±8.92, P=0.16; n=5). KCl‐mediated relaxation was unaffected by L‐NOARG+indomethacin (Emax; 68.1±5.6%, P=0.33; n=5) or the combination of L‐NOARG/indomethacin/ChTx/apamin (Emax; 86.61±14.02%, P=0.35; n=6). In contrast, the combination of L‐NOARG, indomethacin, ouabain and BaCl2 abolished this response (Emax, 5.67±2.59%, P<0.0001, n=6). The characteristics of KCl‐mediated relaxation differed from those of the nitric oxide/prostaglandin‐independent component of the response to ACh, and were endothelium‐dependent, indicating that K+ does not act as an EDHF in human subcutaneous resistance arteries.
影响因子：
--
作者：
BRAYDEN, JE
通讯作者：
BRAYDEN, JE
影响因子：
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作者：
NAGAO, T;ILLIANO, S;VANHOUTTE, PM
通讯作者：
VANHOUTTE, PM