Persistent vascular dysfunction following an acute nonpharmacological reduction in blood pressure in hypertensive patients.
Persistent vascular dysfunction following an acute nonpharmacological reduction in blood pressure in hypertensive patients.
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DOI：
10.1097/hjh.0000000000003104
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发表时间：
2022-06-01
影响因子：
4.9
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中科院分区：
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血管功能障碍是心血管疾病的一个独立危险因素，尽管抗高血压药物可改善血压控制，但高血压患者的血管功能障碍往往持续存在。由于这些药物中的一些可能直接影响血管功能，本研究试图全面检查通过非药物方法（限钠5天）降低血压对22名高血压患者（14名男性/8名女性，50±10岁）血管功能的影响。停药2周后，完成两个为期5天的饮食阶段，自由钠（LS，200 mmol/d），然后限制钠（RS，10 mmol/d）。通过肱动脉血流介导的扩张（FMD）、反应性充血、渐进性握力运动（HG）和被动腿部运动（PLM）评估静息血压和导管和微血管水平的血管功能。尽管限钠诱导血压下降（LS：141±14/85±9; RS：124±12/79±9 mmHg，收缩压和舒张压均为p<0.01），但FMD（LS：4.6±1.8%; RS：5.1± 2.1%，p=0.27）和反应性充血（LS：548±201; RS：615±206 ml，p=0.08）未发生改变。同样，HG运动期间肱动脉血管舒张在不同条件下没有差异（LS：Δ 0.36±0.19 mm; RS：Δ 0.42±0.18 mm，p=0.16）。最后，PLM诱导的峰值血流量变化（LS：5.3±2.5; RS：5.8± 3.6 ml/min/mmHg，p=0.30）和总血管舒张反应（LS：2.0[0.9-2.5] vs. RS：1.7[1.1-2.6]ml/min/mmHg; p = 0.5）在不同条件下也无差异。因此，血管功能障碍，在管道和微血管水平，持续存在于高血压患者，即使血压是急性降低的非药物方法。
Vascular dysfunction, an independent risk factor for cardiovascular disease, often persists in patients with hypertension, despite improvements in blood pressure control induced by antihypertensive medications. As some of these medications may directly affect vascular function, this study sought to comprehensively examine the impact of reducing blood pressure, by a non-pharmacological approach (5 days of sodium restriction), on vascular function in 22 hypertensive individuals (14 males/8 females, 50±10 y). Following a 2-week withdrawal of antihypertensive medications, two 5-day dietary phases, liberal sodium (LS, 200 mmol/d) followed by restricted sodium (RS, 10mmol/day), were completed. Resting blood pressure was assessed and vascular function, at both the conduit and microvascular levels, was evaluated by brachial artery flow mediated dilation (FMD), reactive hyperemia, progressive handgrip exercise (HG), and passive leg movement (PLM). Despite a sodium restriction-induced fall in blood pressure (LS: 141±14/85±9; RS 124±12/79±9 mmHg, p<0.01 for both systolic and diastolic blood pressure), FMD (LS: 4.6±1.8%; RS: 5.1±2.1%, p=0.27), and reactive hyperemia (LS: 548±201; RS: 615±206 ml, p=0.08) were not altered. Similarly, brachial artery vasodilation during HG exercise was not different between conditions (LS: Δ 0.36±0.19 mm; RS: Δ 0.42±0.18 mm, p=0.16). Lastly, PLM-induced changes in peak blood flow (LS: 5.3±2.5; RS: 5.8±3.6ml/min/mmHg, p=0.30) and the total vasodilatory response (LS: 2.0[0.9–2.5] vs. RS: 1.7[1.1–2.6]ml/min/mmHg; p = 0.5) were also not different between conditions. Thus, vascular dysfunction, at both the conduit and microvascular levels, persists in patients with hypertension even when blood pressure is acutely reduced by a non-pharmacological approach.