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人类轻度高钠血症诱导的利钠作用。

Natriuresis induced by mild hypernatremia in humans.

作者信息

Andersen Lars Juel, Andersen Jens Lundbaek, Pump Bettina, Bie Peter

机构信息

Department of Medical Physiology, Panum Institute, University of Copenhagen, DK-2200 Copenhagen, Denmark.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2002 Jun;282(6):R1754-61. doi: 10.1152/ajpregu.00732.2001.

DOI:10.1152/ajpregu.00732.2001
PMID:12010758
Abstract

The hypothesis that increases in plasma sodium induce natriuresis independently of changes in body fluid volume was tested in six slightly dehydrated seated subjects on controlled sodium intake (150 mmol/day). NaCl (3.85 mmol/kg) was infused intravenously over 90 min as isotonic (Iso) or as hypertonic saline (Hyper, 855 mmol/l). After Hyper, plasma sodium increased by 3% (142.0 +/- 0.6 to 146.2 +/- 0.5 mmol/l). During Iso a small decrease occurred (142.3 +/- 0.6 to 140.3 +/- 0.7 mmol/l). Iso increased estimates of plasma volume significantly more than Hyper. However, renal sodium excretion increased significantly more with Hyper (291 +/- 25 vs. 199 +/- 24 micromol/min). This excess was not mediated by arterial pressure, which actually decreased slightly. Creatinine clearance did not change measurably. Plasma renin activity, ANG II, and aldosterone decreased very similarly in Iso and Hyper. Plasma atrial natriuretic peptide remained unchanged, whereas plasma vasopressin increased with Hyper (1.4 +/- 0.4 to 3.1 +/- 0.5 pg/ml) and decreased (1.3 +/- 0.4 to 0.6 +/- 0.1 pg/ml) after Iso. In conclusion, the natriuretic response to Hyper was 50% larger than to Iso, indicating that renal sodium excretion may be determined partly by plasma sodium concentration. The mechanism is uncertain but appears independent of changes in blood pressure, glomerular filtration rate, the renin system, and atrial natriuretic peptide.

摘要

在六名轻度脱水且坐姿的受试者中,对血浆钠升高可独立于体液量变化而诱导利钠作用的假说进行了测试,这些受试者的钠摄入量受到控制(150 mmol/天)。以等渗(Iso)或高渗盐水(Hyper,855 mmol/l)的形式在90分钟内静脉输注NaCl(3.85 mmol/kg)。输注Hyper后,血浆钠升高了3%(从142.0±0.6 mmol/l升至146.2±0.5 mmol/l)。输注Iso期间出现了小幅下降(从142.3±0.6 mmol/l降至140.3±0.7 mmol/l)。Iso使血浆容量估计值的增加显著多于Hyper。然而,Hyper使肾钠排泄量的增加显著更多(291±25对199±24 μmol/分钟)。这种过量并非由动脉压介导,实际上动脉压略有下降。肌酐清除率没有明显变化。Iso和Hyper中血浆肾素活性、ANG II和醛固酮的下降非常相似。血浆心钠素保持不变,而血浆血管加压素在Hyper后升高(从1.4±0.4升至3.1±0.5 pg/ml),在Iso后下降(从1.3±0.4降至0.6±0.1 pg/ml)。总之,对Hyper的利钠反应比对Iso大50%,表明肾钠排泄可能部分由血浆钠浓度决定。其机制尚不确定,但似乎独立于血压、肾小球滤过率、肾素系统和心钠素的变化。

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