Normotensive Salt-sensitive Subjects Research Articles

P597Endothelial dysfunction, arterial stiffness and cardiovascular risk in normotensive salt sensitive subjects

P597Endothelial dysfunction, arterial stiffness and cardiovascular risk in normotensive salt sensitive subjects

Potassium supplementation ameliorates increased plasma homocysteine induced by salt loading in normotensive salt-sensitive subjects

ABSTRACTThe mechanism by which high-salt and low-potassium diet contributes to hypertension remains poorly understood. Plasma homocysteine (Hcys) is recognized as a primary mediator of blood pressure (BP) response to some diets. Therefore, the present study tried to investigate whether plasma Hcys and BP could be regulated by salt loading in normotensive salt-sensitive (SS) persons, and further explored whether potassium supplementation could reverse the effect. We enrolled 47 normotensive subjects, aged 29–65 years. The protocol included 7 days on a low-salt diet (3g/day, NaCl), 7 days on a high-salt diet (18g/day), and then a high-salt diet with potassium supplementation (4.5g/day) for 7 days. After high-salt intake, BP was significantly increased and potassium supplementation lowered it in the SS group. Plasma Hcys were higher in SS subjects than in salt-resistant (SR) subjects after salt loading (34.4 ± 17.0 μmol/L versus 19.16 ± 6.4 μmol/L, P < 0.01). Plasma Hcys in SS subjects was increased on a high-salt diet than on a low-salt diet (34.4 ± 17.0 μmol/L versus 16.5 ± 8.3 μmol/L, P < 0.01), but plasma Hcys was ameliorated by potassium supplementation (34.4 ± 17.0 μmol/L versus 20.9 ± 10.4 μmol/L, P < 0.01). In SS subjects, the change of mean arterial blood pressure (MBP) correlated significantly and positively with the alteration of plasma Hcys during low-salt to high-salt intake and high-salt to high-salt with potassium supplementation (r = 0.75, P < 0.001; r = 0.74, P < 0.001, respectively). Our results indicate that Hcys may partly mediate the impact of high-salt intake and potassium supplementation on BP in SS subjects.

Effect of Salt Intake on Serum Glucagon-Like Peptide-1 Levels in Normotensive Salt-Sensitive Subjects

Background/Aims: Excess dietary salt is a critical risk factor of salt-sensitive hypertension. Glucagon-like peptide-1 (GLP-1) , a gut incretin hormone, conferring benefits for blood pressure by natriuresis and diuresis. We implemented a randomized trial to verify the effect of altered salt intake on serum GLP-1 level in human beings. Methods: The 38 subjects were recruited from a rural community of Northern China. All subjects were sequentially maintained a baseline diet period for 3 days, a low-salt diet period for 7 days (3.0g/day of NaCl) , and a high-salt diet period for additional 7 days (18.0g/day of NaCl). Results: Serum GLP-1 level increased significantly with the change from the baseline period to the low-salt diet period and decreased with the change from the low-salt to high-salt diet in normotensive salt-sensitive (SS) but not salt-resistant (SR) individuals. There was a significant inverse correlation between the serum GLP-1 level and the MAP in SS subjects. Inverse correlation between the serum GLP-1 level and 24-h urinary sodium excretion was also found among different dietary interventions in SS subjects. Conclusions: Our study indicates that variations in dietary salt intake affect the serum GLP-1 level in normotensive salt-sensitive Chinese adults.

HIGH SALT INTAKE FAIL TO ENHANCE PLASMA ADIPONECTIN IN NORMOTENSIVE SALT-SENSITIVE SUBJECTS

ObjectivesEvidences show that salt could modulate adiponectin and inflammation level in normal individuals. Therefore, we hypothesised that abnormalities of adiponectin and inflammation may be the potential mechanism of salt sensitivity....

High salt intake fails to enhance plasma adiponectin in normotensive salt-sensitive subjects

ObjectiveEvidence shows that salt can modulate adiponectin and inflammation levels in normal individuals. Therefore, we hypothesized that abnormalities in adiponectin and inflammation might be the potential mechanism of salt sensitivity. The aim of this study was to investigate whether different alterations of adiponectin and inflammation levels in response to a high-salt intake were exhibited between normotensive salt-sensitive and salt-resistant subjects. MethodsThirty normotensive subjects (25 to 50 y old) were selected from a rural community of northern China. They were sequentially maintained on a normal diet for 3 d at baseline, a low-salt diet for 7 d (NaCl 3 g/d), and then a high-salt diet for 7 d (18 g/d). ResultsSalt sensitivity was diagnosed in 10 subjects who exhibited an increase of at least 10% in mean blood pressure from the low-salt to the high-salt periods. Plasma adiponectin was significantly higher with the high-salt intake than with the low-salt intake (6.1 ± 1.3 versus 7.1 ± 1.7 μg/mL, P = 0.047) in normotensive salt-resistant subjects but not in the normotensive salt-sensitive subjects (6.4 ± 2 versus 5.9 ± 2.1 μg/mL, P = 0.481). The high-salt intake markedly increased plasma tumor necrosis factor-α (P < 0.0001) and monocyte chemoattractant protein-1 (P < 0.0001) in normotensive salt-sensitive and salt-resistant subjects. No significant change in plasma high-sensitivity C-reactive protein was observed. ConclusionsOur data indicate that the disturbance of adiponectin exists in normotensive salt-sensitive subjects during a high-salt diet, which may be a novel underlying mechanism of salt sensitivity.

High salt intake fails to enhance plasma adiponectin in normotensive salt-sensitive subjects

High salt intake fails to enhance plasma adiponectin in normotensive salt-sensitive subjects

Endothelial dysfunction in normotensive salt-sensitive subjects

Salt-sensitivity is associated with a more severe target organ injury and higher mortality, even in normotensive subjects. As endothelial dysfunction is predictive for future cardiovascular events, we evaluated whether normotensive salt-sensitive (NSS) subjects have more pronounced endothelial dysfunction compared with normotensive salt-resistant (NSR) subjects. Normotensive subjects (n=99, aged 25-50 years) were selected from a rural community in northern China. Salt sensitivity was assigned if mean BP increased by ≥10% from a 1-week high salt (18 g/day, NaCl) to low-salt diet (3 g/day, NaCl). Endothelial function was assessed by testing the flow-mediated dilatation (FMD) of the brachial artery using high-resolution ultrasound, as well as nitrogen oxide (NOx) levels, in plasma and urine at baseline. Blood pressure at baseline was similar between NSS and NSR subjects, but diverged during salt intervention. Furthermore, FMD was significantly lower in 17 NSS subjects (10.2±2.5 vs 14.5±1.6%, P=0.037) compared with NSR subjects. In addition, average plasma NOx levels were lower in NSS subjects than NSR subjects (61.2±3.23 μM vs 82.5±1.61 μM, P=0.034). Moreover, Both FMD and plasma NOx levels were negatively correlated with the degree of salt sensitivity (r=-0.435 and r=-0.459, respectively, P<0.01). However, there was no difference in urine NOx between the two groups. Our study indicates that endothelial dysfunction could contribute to the long-term higher levels of target organ injury and higher mortality observed in NSS subjects.

The changes of arterial elasticity in normotensive salt sensitive subjects under salt-loading

Background Salt sensitivity is implicated as a risk factor for cardiovascular disease. We hypothesized that salt loading would influence the arterial elasticity which could reflect endothelium function. The aim of the study was to investigate the different changes of arterial elasticity under high salt dietary intervention between salt sensitive subjects and non-salt sensitive subjects. Methods A 7-day low-sodium (51.3 mmol sodium/day) followed by a 7-day high-sodium (307.8 mmol sodium/day) dietary intervention was conducted among 31 normotensive subjects. BP measurements were obtained at a baseline examination and following the low-sodium and high-sodium interventions using a random-zero sphygmomanometer. Salt sensitivity was defined as the absolute changes in mean arterial pressure (MAP) from baseline to low-sodium and high-sodium interventions. The arterial elasticity was determined by CVProfilor DO-2020 and expressed as elasticity indexes (C(1)—large artery and C(2)—small artery). Results There were 10 subjects recognized as salt sensitive. During low salt intervention, there were no differences in BP and in large and small arterial elasticity indices between salt sensitive subjects and non-salt sensitive subjects (C1: 14.3±1.17 (SS) vs 14.4±0.81 (NSS); C2: 5.2±0.7 (SS) vs 5.4±0.7 (NSS)). After the 7-day high-sodium dietary intervention, the changes of large artery elasticity (C(1)) in salt sensitive subjects were significantly reduced (2.45±0.45 (SS) vs 0.87±0.78 (NSS) ml mm Hg (−1)x 10, P=0.004), but the small artery elasticity (C(2)) was not found to have significant changes neither in salt sensitive subjects nor in salt insensitive subjects (4.7±2.4 (SS) vs 5.4±2.1 (NSS) ml mm Hg (−1)x 100, P=0. 41). Conclusions Our study indicates that short-term salt loading could reduce the large artery elasticity in salt sensitive subjects, but not in non-salt sensitive subjects. Further study is needed to confirm that long-term high salt can reduce both arterial elasticities (C1 and C2).

Salt sensitivity, pulse pressure, and death in normal and hypertensive humans.

Although factors such as age, blood pressure, and its responsiveness to changes in sodium balance and extracellular fluid volume status (salt sensitivity) are associated with an increased risk of end-organ disease and cardiovascular events in hypertensive subjects, no such relationship with mortality has been demonstrated for salt sensitivity in normotensive subjects. We conducted long-term follow-up of 430 normal and 278 hypertensive subjects in whom assessment of salt sensitivity of blood pressure was performed as long as 27 years ago. We ascertained the status of 596 subjects (85% of the total population), 123 (21%) of whom had died. The following initial measurements were significantly (P<0.002) associated with subjects who had died compared with subjects known to be alive: age at study, pulse pressure, systolic, diastolic, and mean arterial pressures, hypertension, salt sensitivity, baseline renin levels, and body mass index (but not body weight). A stepwise logistic regression found the following independent predictors of death (odds ratio, 95% CI): age at initial study (1.08, 1.06 to 1.10), baseline blood pressure (1.03, 1.01 to 1.04), sodium sensitivity (1.73, 1.02 to 2.94), and male gender (1.91, 1.15 to 3.17). When survival curves were examined, normotensive salt-sensitive subjects aged >25 years when initially studied were found to have a cumulative mortality similar to that of hypertensive subjects, whereas salt-resistant normotensive subjects had increased survival (P:<0.001). These observations provide unique evidence of a relationship between salt sensitivity and mortality that is independent of elevated blood pressure.

Renal acid-base excretion in normotensive salt-sensitive humans.

Reduced extracellular pH and bicarbonate levels recently have been reported in normotensive salt-sensitive subjects. To assess the possible role of altered renal acid-base handling in the perturbation of acid-base status in these individuals, we measured the renal acid-base excretion after an acute oral administration of either an alkali or acid load in normotensive salt-sensitive and salt-resistant men. Twenty-four young (22 to 29 years old), healthy male volunteers were placed on a low-salt diet (20 mmol NaCl per day) for 2 weeks with either 220 mmol NaCl or placebo added to the low-salt diet for 1 week each in a randomized single-blind crossover order. Salt sensitivity was defined as a significant drop in mean arterial pressure (> 3 mm Hg, mean of 60 readings taken on the seventh day of each diet, P < .05) during the low-salt diet. On the fifth and seventh days of each week, subjects were given an oral load of either sodium citrate (0.7 mmol/kg) or ammonium chloride (2.2 mmol/kg), respectively, in a randomized order, and arterial and urinary acid-base status was assessed at baseline and followed for 8 hours thereafter. According to the above definition, 13 subjects were considered salt sensitive. During the high-salt diet, mean arterial pressure was higher in the salt-sensitive than in the salt-resistant group (P < .01). Cumulative urinary bicarbonate excretion after the administration of sodium citrate was lower in the salt-sensitive than in the salt-resistant subjects during both the low-salt (46%, P < .001) and high-salt (32%, P < .01) diets.(ABSTRACT TRUNCATED AT 250 WORDS)