Division of Kinesiology, Faculty of Health, School of Health and Human Performance, Dalhousie University, Halifax, Nova Scotia, Canada.
J Appl Physiol (1985). 2021 Jan 1;130(1):17-25. doi: 10.1152/japplphysiol.00698.2020. Epub 2020 Oct 29.
Heterogeneous flow-mediated dilation (FMD) and low-flow-mediated constriction (L-FMC) responses have been reported between upper- and lower-limb arteries. Radial artery L-FMC, but not FMD, responses are blunted when endothelial-derived hyperpolarizing factors (EDHFs) or prostaglandin production is inhibited in young adults. However, it is unknown if these mechanisms similarly impact endothelial-dependent responses in the brachial (BA) and popliteal (POP) arteries. We tested whether BA- and POP-L-FMC and FMD would be influenced by independent EDHF and prostaglandin inhibition. Eighteen participants (23 ± 3 yr; 6♀) completed three randomized and double-blinded ultrasound assessments following ingestion of an opaque capsule containing maltodextrin (control), 150 mg of fluconazole (EDHF inhibition), or 500 mg of aspirin (prostaglandin inhibition). POP resting diameter was reduced following fluconazole administration (6.13 ± 0.63 mm vs. 6.19 ± 0.65 mm in control, = 0.03). Compared with control, fluconazole also blunted the relative L-FMC responses in both the BA (-2.1 ± 0.8% vs. -0.8 ± 1.0%, = 0.001) and POP (-1.7 ± 1.1% vs. -0.8 ± 0.9%, = 0.009). In contrast, aspirin did not impact either the BA (-1.9 ± 0.7%) or POP-L-FMC (-1.3 ± 0.6%) responses (both, > 0.35). The FMD response was unchanged following fluconazole or aspirin administration in either artery (both, > 0.36). Our findings demonstrate that EDHF mediates L-FMC responses in both the brachial and popliteal arteries. Complementary to the nitric oxide-mediated FMD response, L-FMC appears to provide information regarding the EDHF pathway. Future research should uncover if these mechanisms impact older adults and/or patient populations characterized by vascular endothelial dysfunction associated with low aerobic fitness and habitual physical activity levels. We compared changes in upper- and lower-limb artery endothelial-dependent vasodilatory and vasoconstrictor responses between control, prostaglandin inhibition, and endothelial-derived hyperpolarizing factor inhibition conditions. Neither prostaglandins nor endothelial-derived hyperpolarizing factor influenced flow-mediated dilation responses in either the brachial or popliteal artery. In contrast, endothelial-derived hyperpolarizing factor, but not prostaglandins, reduced resting brachial artery blood flow and shear rate and resting popliteal artery diameter, as well as low-flow-mediated constriction responses in both the popliteal and brachial arteries.
已有研究报道，在上肢和下肢动脉之间存在异质性血流介导的扩张（FMD）和低血流介导的收缩（L-FMC）反应。在年轻成年人中，当抑制内皮衍生超极化因子（EDHF）或前列腺素的产生时，桡动脉 L-FMC 而不是 FMD 反应会减弱。然而，目前尚不清楚这些机制是否同样影响肱动脉（BA）和腘动脉（POP）内皮依赖性反应。我们检测了 BA 和 POP-L-FMC 和 FMD 是否会受到独立的 EDHF 和前列腺素抑制的影响。18 名参与者（23±3 岁；6 名女性）在摄入含有麦芽糊精的不透明胶囊（对照）、150mg 氟康唑（EDHF 抑制）或 500mg 阿司匹林（前列腺素抑制）后完成了三次随机、双盲超声评估。氟康唑给药后，POP 静息直径减小（6.13±0.63mm 与对照中的 6.19±0.65mm， = 0.03）。与对照相比，氟康唑还减弱了 BA（-2.1±0.8%比-0.8±1.0%， = 0.001）和 POP（-1.7±1.1%比-0.8±0.9%， = 0.009）中的相对 L-FMC 反应。相比之下，阿司匹林并未影响 BA（-1.9±0.7%）或 POP-L-FMC（-1.3±0.6%）反应（均 > 0.35）。在 BA 或 POP 中，氟康唑或阿司匹林给药后 FMD 反应均未改变（均 > 0.36）。我们的研究结果表明，EDHF 介导了 BA 和 POP 动脉中的 L-FMC 反应。与一氧化氮介导的 FMD 反应互补，L-FMC 似乎提供了关于 EDHF 途径的信息。未来的研究应该揭示这些机制是否会影响与低有氧健身和习惯性体力活动水平相关的血管内皮功能障碍的老年人和/或患者群体。我们比较了在对照、前列腺素抑制和内皮衍生超极化因子抑制条件下，上下肢动脉内皮依赖性血管扩张和血管收缩反应的变化。前列腺素和内皮衍生超极化因子均不影响肱动脉或腘动脉的血流介导的扩张反应。相比之下，内皮衍生超极化因子而非前列腺素降低了肱动脉的静息血流和剪切率以及静息腘动脉直径，并降低了 POP 和 BA 动脉的低血流介导的收缩反应。
