高醛固酮和低n端心房钠素原肽作为社区盐敏感性的生物标志物。

Wolfgang Lieb, Michael J Pencina, Paul F Jacques, Thomas J Wang, Martin G Larson, Daniel Levy, William B Kannel, Ramachandran S Vasan
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引用次数: 14

摘要

背景:盐敏感性是一种以饮食盐摄入量增加导致血压升高为特征的特征,它与心血管靶器官损伤和心血管疾病事件的高发率相关。最近的实验研究强调了利钠肽和醛固酮在调节盐敏感性中的潜在作用。设计:前瞻性队列研究。方法:我们评估了1575名非高血压的Framingham Offspring队列参与者(平均年龄55±9岁,58%为女性),他们接受了循环醛固酮和n端心房钠肽(NT-ANP)的常规测量,并评估了饮食钠摄入量。如果参与者的血清醛固酮>性别特异性中值,但血浆NT-ANP≤性别特异性中值,则被归类为潜在的“盐敏感”。膳食钠摄入量被分类为低钠和高钠(按性别特异性中位数进行二分)。我们使用多变量线性回归将盐敏感性(如上定义)与随访(中位4年)收缩压和舒张压的纵向变化(Δ)联系起来。结果:“盐敏感”的参与者(N = 437)血压显著升高(Δ收缩压,+4.4和+2.3 mmHg;Δ舒张,+1.9和-0.3 mmHg;与其他参与者相比(Δ收缩压,+2.8和+1.0 mmHg;Δ舒张,+0.5和-0.2 mmHg;高钠饮食和低钠饮食;各组间Δ收缩压和Δ舒张压差异P = 0.033和P = 0.0127)。结论:我们的观察数据表明,较高的循环醛固酮和较低的NT-ANP浓度可能是社区盐敏感性的标志。需要进一步的研究来证实这些观察结果。
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Higher aldosterone and lower N-terminal proatrial natriuretic peptide as biomarkers of salt sensitivity in the community.

Background: Salt sensitivity, a trait characterized by a pressor blood pressure response to increased dietary salt intake, has been associated with higher rates of cardiovascular target organ damage and cardiovascular disease events. Recent experimental studies have highlighted the potential role of the natriuretic peptides and aldosterone in mediating salt sensitivity.

Design: Prospective cohort study.

Methods: We evaluated 1575 non-hypertensive Framingham Offspring cohort participants (mean age 55 ± 9 years, 58% women) who underwent routine measurements of circulating aldosterone and N-terminal proatrial natriuretic peptide (NT-ANP) and assessment of dietary sodium intake. Participants were categorized as potentially 'salt sensitive' if their serum aldosterone was >sex-specific median but plasma NT-ANP was ≤sex-specific median value. Dietary sodium intake was categorized as lower versus higher (dichotomized at the sex-specific median). We used multivariable linear regression to relate presence of salt sensitivity (as defined above) to longitudinal changes (Δ) in systolic and diastolic blood pressure on follow-up (median four years).

Results: Participants who were 'salt sensitive' (N = 437) experienced significantly greater increases in blood pressure (Δ systolic, +4.4 and +2.3 mmHg; Δ diastolic, +1.9 and -0.3 mmHg; on a higher versus lower sodium diet, respectively) as compared to the other participants (Δ systolic, +2.8 and +1.0 mmHg; Δ diastolic, +0.5 and -0.2 mmHg; on higher versus lower sodium diet, respectively; P = 0.033 and P = 0.0127 for differences between groups in Δ systolic and Δ diastolic blood pressure, respectively).

Conclusions: Our observational data suggest that higher circulating aldosterone and lower NT-ANP concentrations may be markers of salt sensitivity in the community. Additional studies are warranted to confirm these observations.

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