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Increased Aortic Characteristic Impedance Explains Relations Between Urinary Na + /K + and Pulse or Systolic Blood Pressure
Hypertension ( IF 8.3 ) Pub Date : 2020-05-01 , DOI: 10.1161/hypertensionaha.119.14563
Keneilwe N. Mmopi 1 , Gavin R. Norton 1 , Hamza Bello 1 , Carlos Libhaber 1 , Mohlabani Masiu 1 , Daniel Da Silva Fernandes 1 , Pinhas Sareli 1 , Vernice Peterson 1 , Angela J. Woodiwiss 1
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Supplemental Digital Content is available in the text. Alterations in sodium (Na+) relative to potassium (K+) intake increase systolic blood pressure, effects in-part attributed to enhanced pulsatile loads (pulse pressure) beyond steady-state pressures (mean arterial pressure). Whether this effect is through reversible changes (increases in blood volume and hence aortic flow [Q] or wave reflection [Pb]), or potentially irreversible structural changes in the proximal aorta, is unknown. In 581 black South Africans, we determined 24-hour urinary Na+ and K+ excretion and aortic function from central aortic pressure (radial pulse wave analysis [SphygmoCor software]), velocity, and diameter measurements. Proximal aortic function was assessed from characteristic impedance (Zc). Beyond mean arterial pressure and additional confounders, urinary Na+/K+ was independently associated with Zc (P<0.005) but not peak aortic Q (P=0.30) or alternative aspects of Q or ejection volume. Although age was strongly associated with proximal aortic diameter, no independent relations between urinary Na+/K+ and aortic diameter were noted (P=0.17). Relations between urinary Na+/K+ and Zc translated into independent relations with early systolic compression wave pressures (QxZc [PQxZc]) and aortic forward wave pressures but not Pb. Moreover, neither reflected wave magnitude (P=0.92) nor aortic pulse wave velocity were independently associated with urinary Na+/K+. In product of coefficient mediation analysis, the independent relations between urinary Na+/K+ and peak aortic or brachial pulse pressure or systolic blood pressure were accounted for by Zc and PQxZc. In conclusion, abnormalities in Na+/K+ intake determine pulse pressure or systolic blood pressure beyond mean arterial pressure mainly through potentially irreversible impacts on proximal aortic impedance rather than readily modifiable increases in aortic flow (blood volume) or wave reflection.

中文翻译:

增加的主动脉特征阻抗解释了尿 Na + /K + 与脉搏或收缩压之间的关系

补充数字内容在文本中可用。钠 (Na+) 相对于钾 (K+) 摄入量的变化会增加收缩压,其影响部分归因于超过稳态压力(平均动脉压)的增强的脉动负荷(脉搏压力)。这种影响是通过可逆的变化(血容量增加,从而增加主动脉流量 [Q] 或波反射 [Pb]),还是通过近端主动脉的潜在不可逆结构变化,尚不清楚。在 581 名南非黑人中,我们通过中心主动脉压(径向脉搏波分析 [SphygmoCor 软件])、速度和直径测量值确定了 24 小时尿 Na+ 和 K+ 排泄和主动脉功能。从特征阻抗 (Zc) 评估近端主动脉功能。除了平均动脉压和其他混杂因素之外,尿 Na+/K+ 与 Zc (P<0.005) 独立相关,但与峰值主动脉 Q (P=0.30) 或 Q 或射血量的其他方面无关。尽管年龄与近端主动脉直径密切相关,但未发现尿 Na+/K+ 与主动脉直径之间存在独立关系(P=0.17)。尿 Na+/K+ 和 Zc 之间的关系转化为与早期收缩期压缩波压力 (QxZc [PQxZc]) 和主动脉前向波压力但不是 Pb 的独立关系。此外,反射波幅度 (P=0.92) 和主动脉脉搏波速度都与尿 Na+/K+ 无关。在系数中介分析的产物中,尿 Na+/K+ 与峰值主动脉或肱动脉脉压或收缩压之间的独立关系由 Zc 和 PQxZc 解释。综上所述,
更新日期:2020-05-01
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