Hemodynamic effects of dietary sodium in man: a preliminary report.

Sullivan, Jay M.; Ratts, Thomas E.; Taylor, John; Kraus, Dietmar; Barton, B R; Patrick, Darrell R.; Reed, S.

doi:10.1161/01.hyp.2.4.506

Cited by 100 publications

(32 citation statements)

References 22 publications

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“…4 " 13 In the present study, we found the prevalence of sodium sensitivity to be approximately 16% in normotensive subjects and 29% in subjects with borderline hypertension. Subsequently, Weinberger et al 8 and Luft and Weinberger 10 noted that the prevalence of sodium sensitivity was higher in hypertensive than in normotensive groups.…”

Section: Discussionsupporting

confidence: 53%

“…4 ' 13 -"• 18 Stroke volume was determined by subtracting the systolic from diastolic volumes. Cardiac output was calculated as the product of simultaneous heart rate and stroke volume averaged over 10 seconds.…”

Section: Echocardiographic Studiesmentioning

confidence: 99%

“…3 Over the past several years, a number of investigators have demonstrated that only a portion of normotensive and hypertensive groups display a change in blood pressure when sodium-depleted or sodium-loaded. 4 " 12 The mechanisms responsible for sodium sensitivity remain to be clarified.…”

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Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Sullivan

Ratts

1988

Hypertension

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SUMMARY To investigate factors associated with sodium sensitivity, 157 subjects were studied while receiving 10 and 200 mEq sodium diets. Measurements included blood pressure (BP), forearm vascular resistance, plasma renin activity (PRA), and plasma aldosterone. Sodium repletion was associated with a greater than 5% increase in mean BP in 16% of the normotensive subjects and 29% of the borderline hypertensive subjects. Sodium-sensitive subjects were compared with sodiumresistant subjects in both the normotensive (n = 92) and borderline hypertensive (n = 65) groups. Forearm vascular resistance was significantly higher (p<0.05) during sodium loading in the sodiumsensitive subgroups of both the normotensive and borderline hypertensive groups (35.8 ± 29 vs 23.8 ± 20 [SD] and 37.5 ± 29 vs 22.5 ± 14 mm Hg/ml/min/100 g, respectively. Venous capacitance was lower in the sodium-sensitive than in the sodium-resistant borderline hypertensive subjects (0.8 ± 0.21 vs 1.69 ± 0.24 ml/100 g). During sodium restriction, PRA was significantly lower (p<0.01) in the sodium-sensitive subsets (2.56 ± 1.6 vs 4.04 ± 2.6; 2.65 ± 2.1 vs 3.88 ± 2.6 ng angiotensin I/ml/hr). Aldosterone was lower (p<0.01) during sodium depletion in the sodium-sensitive subsets (17.3 ± 12 vs 26.3 ± 16; 18.5 ± 18 vs 27.9 ± 17 ng/ml). A significant inverse correlation existed between change in BP with sodium repletion and change in PRA or level of PRA during sodium depletion (p<0.003). We conclude that both normotensive and borderline hypertensive sodiumsensitive subjects are characterized by an increase in forearm vascular resistance during high sodium intake and that this characteristic is associated with decreased responsiveness of the renin-aldosterone system during sodium depletion. (Hypertension 11: 717-723, 1988) KEY WORDS * hypertension • sodium • vascular resistance • hemodynamics renin • aldosterone A LTHOUGH considerable evidence links dietary / \ sodium intake with high blood pressure, sev-A. \ . eral observations suggest that all persons are not affected equally by the hypertensive effects of sodium. By selective inbreeding, Dahl et al.1 have developed strains of rats that become hypertensive when fed a high sodium diet and others that are resistant to the hypertensive effects of sodium. Worldwide studies of sodium intake in various human populations have shown a direct relationship between sodium intake and the prevalence of hypertension, 2 yet in certain populations, the majority of persons remain normotensive despite high sodium intake.3 Over the past several years, a number of investigators have demonstrated

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Section: Discussionsupporting

confidence: 53%

Section: Echocardiographic Studiesmentioning

confidence: 99%

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Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Sullivan

Ratts

1988

Hypertension

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“…[22][23][24][25][26] In addition, our results show that in hypertensives, changes in plasma sodium are related directly to the response of the renin-angiotensin system, which suggests that changes in plasma sodium per se could be a drive that changes plasma renin activity, 27 aldosterone, and atrial natriuretic peptide release that occur with changes in salt intake.…”

Section: Discussionmentioning

confidence: 87%

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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“…There are also different classifications of salt sensitivity. Some investigators consider it necessary to have a mean BP increase of 5% (12), others of 10% (13) from LSD to HSD to classify someone as being salt sensitive. Other investigators prefer to consider absolute values, for example, a mean BP increase of 3 mmHg between diets (14).…”

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confidence: 99%

Salt and insulin sensitivity after short and prolonged high salt intake in elderly subjects

Lima

Tozetto

Lima

et al. 2009

Braz J Med Biol Res

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Salt sensitivity and insulin resistance are correlated with higher cardiovascular risk. There is no information about changes in salt sensitivity (SS) and insulin sensitivity (IS) after a chronic salt overload in humans. The aim of this study was to evaluate these parameters in the elderly. Seventeen volunteers aged 70.5 ± 5.9 years followed a low-salt diet (LSD) for 1 week and a high-salt diet (HSD) for 13 weeks. We evaluated SS after one week (HSD1) and after 13 weeks (HSD13), and subjects’ IS and lipids on their usual diet (UD) at HSD1, and at HSD13. Blood pressure (BP) was measured at each visit and ambulatory blood pressure monitoring (ABPM) was performed twice. SS was the same at HSD1 and HSD13. Systolic BP was lower on LSD than on UD (P = 0.01), HSD1 (P < 0.01) and HSD13 (P < 0.01). When systolic and diastolic BP were evaluated by ABPM, they were higher at HSD13 during the 24-h period (P = 0.03 and P < 0.01) and during the wakefulness period (P = 0.02 and P < 0.01) compared to the UD. Total cholesterol was higher (P = 0.04) at HSD13 than at HSD1. Glucose and homeostasis model assessment (HOMA) were lower at HSD1 (P = 0.02 and P = 0.01) than at HSD13. Concluding, the extension of HSD did not change the SS in an elderly group. The higher IS found at HSD1 did not persist after a longer HSD. A chronic HSD increased BP as assessed by ABPM

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Hemodynamic effects of dietary sodium in man: a preliminary report.

Cited by 100 publications

References 22 publications

Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Plasma Sodium

Salt and insulin sensitivity after short and prolonged high salt intake in elderly subjects

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