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人体高血压患者血浆亚硝酸盐和硝酸盐水平与盐敏感性的关系研究:盐摄入对一氧化氮合成的调节作用

Study on the relationship between plasma nitrite and nitrate level and salt sensitivity in human hypertension : modulation of nitric oxide synthesis by salt intake.

作者信息

Fujiwara N, Osanai T, Kamada T, Katoh T, Takahashi K, Okumura K

机构信息

Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki, Japan.

出版信息

Circulation. 2000 Feb 29;101(8):856-61. doi: 10.1161/01.cir.101.8.856.

Abstract

BACKGROUND

High salt intake suppresses the effect of nitric oxide (NO) in the peripheral resistance vessels in animal models. We tested the hypothesis that the modulation of endogenous NO is related to salt sensitivity in human hypertension.

METHODS AND RESULTS

Inpatients with essential hypertension (n=24) were maintained on a normal-salt diet (12 g/d NaCl) for 3 days, a low-salt diet (2 g), a high-salt diet (20 to 23 g), and a low-salt diet for 7 days. Normotensive subjects (n=16) were maintained on the first 2 salt diets. The hypertensive patients whose average 24-hour blood pressure was increased by >5% by salt loading were assigned to group 1 (n=8) and the others to group 2 (n=16). Nitrate plus nitrite (NO(x)) was measured by the Griess method, and asymmetrical dimethylarginine (ADMA) by high-performance liquid chromatography. The plasma NO(x) level during the normal-salt diet was lower in group 1 than in group 2 and the normotensive group. After salt loading, the plasma NO(x) level was decreased and reversed after the second salt restriction. Plasma ADMA level was increased after salt loading and decreased after salt restriction. The change in plasma NO(x) level was correlated inversely with those in blood pressure (r=-0.59, P=0.0007) and plasma ADMA level (r=-0.64, P=0.003) after salt loading and restriction.

CONCLUSIONS

Modulation of NO synthesis by salt intake may be involved in a mechanism for salt sensitivity in human hypertension, presumably via the change in ADMA.

摘要

背景

在动物模型中,高盐摄入会抑制一氧化氮(NO)在周围阻力血管中的作用。我们检验了内源性NO的调节与人类高血压盐敏感性相关这一假设。

方法与结果

24例原发性高血压住院患者先维持3天正常盐饮食(12克/天氯化钠),接着是低盐饮食(2克)、高盐饮食(20至23克),最后再进行7天低盐饮食。16例血压正常的受试者维持前两种盐饮食。盐负荷后平均24小时血压升高>5%的高血压患者被分配到第1组(n = 8),其他患者被分配到第2组(n = 16)。采用格里斯法测量硝酸盐加亚硝酸盐(NOx),用高效液相色谱法测量不对称二甲基精氨酸(ADMA)。第1组在正常盐饮食期间的血浆NOx水平低于第2组和血压正常组。盐负荷后,血浆NOx水平下降,在第二次盐限制后逆转。盐负荷后血浆ADMA水平升高,盐限制后降低。盐负荷和限制后,血浆NOx水平的变化与血压变化(r = -0.59,P = 0.0007)和血浆ADMA水平变化(r = -0.64,P = 0.003)呈负相关。

结论

盐摄入对NO合成的调节可能参与了人类高血压盐敏感性机制,可能是通过ADMA的变化实现的。

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