An abnormal sodium metabolism in Japanese patients with essential hypertension, judged by serum sodium distribution, renal function and the renin-aldosterone system

Komiya, Ichiro; Yamada, Takashi; Takasu, Nobuyuki; Asawa, Takayuki; Akamine, Hikaru; Yagi, Noriharu; Nagasawa, Yoshitaka; Ohtsuka, Hideyuki; Miyahara, Yasuhiro; Sakai, Hideki; Sato, Akira; Aizawa, Toru

doi:10.1097/00004872-199715010-00006

Cited by 60 publications

(38 citation statements)

References 31 publications

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“…The serum sodium distribution in the hypertensive patients was shifted by Ϸ2 mmol/L toward the higher values. 41 It is possible that some of these differences could be explained by undetected primary aldosteronism in some individuals, but this is unlikely to explain all of the differences. Furthermore, in the study by Bulpitt et al, 38 there was still a significant relationship between plasma sodium and systolic blood pressure after adjusting for potential confounding factors (eg, age, body mass index, serum potassium, calcium, proteins, blood hemoglobin, mean corpuscular volume, and alcohol intake).…”

Section: Discussionmentioning

confidence: 99%

Plasma Sodium

Markandu²,

Sagnella³

et al. 2005

Hypertension

152

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Abstract-Salt intake is a major regulator of blood pressure. There is evidence that those who develop high blood pressure have an underlying defect in the ability of the kidney to excrete salt. It has been suggested that this results in a greater tendency to retain sodium and an increased compensatory response that is responsible for the rise in blood pressure.There is also evidence suggesting that small increases in plasma sodium may directly affect blood pressure, independent of the associated expansion in extracellular volume. We reanalyzed 3 types of studies of changing salt intake.(1) An acute and large reduction in salt intake from 350 mmol/d to 10 to 20 mmol/d for 5 days in hypertensives and normotensives was associated with a fall in plasma sodium of Ϸ3 mmol/L (PϽ0.001). (2) Progressive increases in salt intake from 10 to 250 mmol/d by a daily amount of 50 mmol in normotensives caused increases in plasma sodium (PϽ0.001). (3) Longer-term modest reduction in salt intake in hypertensives was studied in double-blind randomized crossover studies; 1 month of usual salt intake (Ϸ170 mmol/d) compared with reduced salt intake (Ϸ100 mmol/d). There was a decrease in plasma sodium of 0.4Ϯ0.2 mmol/L (PϽ0.05), which was weakly but significantly correlated with the fall in systolic blood pressure (rϭ0.18; PϽ0.05). These studies demonstrate that an increase or a decrease in salt intake causes changes in plasma sodium. Small changes in plasma sodium alter extracellular volume, which may influence blood pressure. Changes in plasma sodium may also affect blood pressure directly. Key Words: plasma Ⅲ sodium Ⅲ blood pressure E levated blood pressure is the major cause of cardiovascular disease (ie, stroke, heart failure, and coronary heart disease). 1,2 A recent World Health Organization report showed that raised blood pressure is responsible for 62% of stroke and 49% of coronary heart disease worldwide. 2 Much evidence from epidemiological, 3 migration, 4 intervention, 5 genetic, 6 and animal studies 7 suggests that salt intake plays an important role in regulating blood pressure. Furthermore, there is increasing evidence that a high salt intake has direct harmful effects on the cardiovascular system (eg, it increases the mass of left ventricular wall, stiffens conduit arteries, and thickens and narrows resistance arteries, independent of and additive to the effect of salt on blood pressure. 8 -12 However, the mechanisms whereby salt raises blood pressure and induces direct cardiovascular organ damage are not clear. Much evidence suggests that in those who develop high blood pressure, there is an underlying defect in the ability of the kidney to excrete salt, and that the greater compensatory response required to restore sodium balance is responsible for the increase in blood pressure. 13 However, the potential role of small changes in plasma sodium has rarely been considered. To look at this further, we reanalyzed 3 types of studies that we conducted on changing salt intake. MethodsThe methods used in the 3 types of salt ...

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Section: Discussionmentioning

confidence: 99%

Plasma Sodium

Markandu²,

Sagnella³

et al. 2005

Hypertension

152

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“…Interestingly, these findings had some parallels with regard to ARR when applied to the hypertensive population. Komiya et al 47 observed that ARR related positively to age and plasma sodium concentration in 741 patients with essential hypertension, relationships which were not detectable using plasma aldosterone levels. 48 A recent study reported by Schlaich et al 49 involving young adults with mild hypertension suggested that there was a linear relationship between poor plasma aldosterone suppression with deterioration of left ventricular diastolic function in response to salt loading.…”

Section: The Issue Is Whether Hyperaldosteronism Varies Inmentioning

confidence: 99%

Is aldosterone the missing link in refractory hypertension?: aldosterone-to-renin ratio as a marker of inappropriate aldosterone activity

2002

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Use of the random aldosterone-to-renin ratio (ARR) as a reliable marker of inappropriate aldosterone activity has led to primary aldosteronism (PA) being increasingly diagnosed in hypertensive patients. At least 10% of hypertensives have been found to have PA, the majority of whom presumably have bilateral adrenal hyperplasia or idiopathic hyperaldosteronism as an aetiology for PA. Whilst these patients clearly have excess aldosterone activity, they have in common many features that are found in hypertensive patients in general, amongst which include heightened angiotensin II adre-

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“…39 The structural changes in intramyocardial coronary arteries induced by a high salt diet are accompanied by a number of metabolic alterations including an increased generation of reactive oxygen species 40 which, among other effects, oxidise nitric oxide thus reducing its dilator effect 41,42 and the arteriolar response to acetylcholine. 40 As a rise in salt intake is usually accompanied by a small rise in plasma sodium and plasma sodium tends to be raised in essential hypertension 43 it is possible that the effect of a small change in sodium concentration on in vitro cultures of endothelial cells may also be relevant to a consideration of the effect of dietary salt on vessels in vivo. For instance increasing the sodium concentration of the culture fluid of cultured myocardial myocytes and vascular smooth muscle by 6 mM/l for 5 days causes hypertrophy.…”

Section: Vesselsmentioning

confidence: 99%

Harmful effects of dietary salt in addition to hypertension

2002

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In addition to raising the blood pressure dietary salt is responsible for several other harmful effects. The most important are a number which, though independent of the arterial pressure, also harm the cardiovascular system. A high salt intake increases the mass of the left ventricle, thickens and stiffens conduit arteries and thickens and narrows resistance arteries, including the coronary and renal arteries. It also increases the number of strokes, the severity of cardiac failure and the tendency for platelets to aggregate. In renal disease, a high salt intake accelerates the rate of renal functional

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An abnormal sodium metabolism in Japanese patients with essential hypertension, judged by serum sodium distribution, renal function and the renin-aldosterone system

Cited by 60 publications

References 31 publications

Plasma Sodium

Plasma Sodium

Is aldosterone the missing link in refractory hypertension?: aldosterone-to-renin ratio as a marker of inappropriate aldosterone activity

Harmful effects of dietary salt in addition to hypertension

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