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首页> 外文期刊>American Journal of Physiology >Evidence for a basal release of a cytochrome-related endothelium-derived hyperpolarizing factor in the radial artery in humans.
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Evidence for a basal release of a cytochrome-related endothelium-derived hyperpolarizing factor in the radial artery in humans.

机译：在人类radial动脉中基础释放细胞色素相关的内皮源超极化因子的证据。

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摘要

Whether a cytochrome P-450 (CYP)-related endothelium-derived hyperpolarizing factor (EDHF), acting through calcium-activated potassium (K(Ca)) channels, interacts with nitric oxide (NO) to regulate the basal diameter of human peripheral conduit arteries is unexplored in vivo. Radial artery diameter (echo tracking) and blood flow (Doppler) were measured, after oral aspirin (500 mg), in eight healthy volunteers during local infusion for 8 min of tetraethylammonium chloride (TEA; 9 micromol/min), as K(Ca) channel inhibitor, and fluconazole (0.4 micromol/min), as CYP inhibitor, alone and in combination with N(G)-monomethyl-L-arginine (L-NMMA; 8 micromol/min), as endothelial NO synthase inhibitor. Endothelium-independent dilatation was assessed by using sodium nitroprusside (SNP). Radial diameter was unaffected by L-NMMA (0.4 +/- 0.9%) and fluconazole (-1.6 +/- 0.8%) but was decreased by TEA (-5.0 +/- 1.0%), L-NMMA + fluconazole (-5.3 +/- 0.5%), and L-NMMA + TEA (-9.9 +/- 1.3%). These effects are still significant even when the concomitant decreases in blood flow induced by L-NMMA (-24 +/- 4%), TEA (-21 +/- 3%), L-NMMA + fluconazole (-26 +/- 5%), and L-NMMA + TEA (-35 +/- 4%) were taken as covariate into analysis. Conversely, fluconazole alone slightly but not significantly increased radial flow (13 +/- 6%). L-NMMA alone or with TEA and with fluconazole enhanced radial artery dilatation to SNP, whereas TEA and fluconazole alone did not modify this response. These results confirm in humans the involvement of NO and K(Ca) channels in the regulation of basal conduit artery diameter. Moreover, the synergistic effect of combined inhibition of NO synthesis and CYP on the decrease in radial diameter in the absence of such effect after L-NMMA and fluconazole alone unmasks the role of CYP in this regulation and shows the presence of an interaction between NO and a CYP-related EDHF to maintain peripheral conduit artery diameter in vivo. Furthermore, the higher vasoconstrictor effect of TEA compared with fluconazole suggests that different K(Ca) channel-dependent hyperpolarizing mechanisms could exist in conduit arteries.
机译：细胞色素P-450（CYP）相关的内皮衍生的超极化因子（EDHF）是否通过钙激活的钾（K（Ca））通道与一氧化氮（NO）相互作用以调节人体外周导管的基础直径体内动脉尚未开发。口服阿司匹林（500毫克）后，在八名健康志愿者局部输注氯化四乙铵（TEA; 9微摩尔/分钟）的过程中，测量了八名健康志愿者的动脉直径（回波追踪）和血流量（多普勒），以K（Ca通道抑制剂）和氟康唑（0.4 micromol / min）作为CYP抑制剂，单独或与N（G）-单甲基-L-精氨酸（L-NMMA; 8 micromol / min）组合作为内皮一氧化氮合酶抑制剂。通过使用硝普钠（SNP）评估非内皮依赖性扩张。径向直径不受L-NMMA（0.4 +/- 0.9％）和氟康唑（-1.6 +/- 0.8％）的影响，但受TEA（-5.0 +/- 1.0％），L-NMMA +氟康唑（-5.3）的影响而减小+/- 0.5％）和L-NMMA + TEA（-9.9 +/- 1.3％）。即使伴随L-NMMA（-24 +/- 4％），TEA（-21 +/- 3％），L-NMMA +氟康唑（-26 +/-）引起的血流减少，这些作用仍然显着5％）和L-NMMA + TEA（-35 +/- 4％）作为协变量进行分析。相反，单独使用氟康唑则略有增加，但径向流量却没有明显增加（13 +/- 6％）。单独使用L-NMMA或与TEA和氟康唑一起使用可增强radial动脉向SNP的扩张，而仅TEA和氟康唑则不会改变这种反应。这些结果在人类中证实了NO和K（Ca）通道参与了基底导管动脉直径的调节。此外，在单独使用L-NMMA和氟康唑后，没有抑制NO合成和CYP的协同作用对on径减小的协同作用掩盖了CYP在此调节中的作用，并显示了NO和CYP之间存在相互作用。 CYP相关的EDHF以维持体内外周导管动脉直径。此外，与氟康唑相比，TEA的血管收缩作用更高，这表明导管动脉中可能存在不同的K（Ca）通道依赖性超极化机制。

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