Low Salt Intake Research Articles

64 LOW SALT DIET AFFECTS ANGIOTENSIN RECEPTOR REGULATION ON MONOCYTES AND NEUTROPHILS IN HUMANS

Background: Angiotensin II (Ang II) is a key player in hypertension, inflammation and oxidative stress and atherosclerosis. Circulating cells reportedly express AT1 receptors (AT1R). In the present study we assessed AT1R and AT2R in monocytes (MONO) and neutrophils (NEUTRO) during manipulations in salt intake and upon ex vivo cytokine and Ang II stimulation in healthy humans. Methods and results: MONO, NEUTRO more than B-cells, but not T-cells, expressed AT1R AT2R assessed by FACS on fresh whole blood (n = 10). Sodium excretion was 145±37/d, 18±15 mmol/d and 197±81 mmol/d at baseline, low salt and high salt (P<0.01). Low salt did not affect MONO or NEUTRO AT1R or AT2R expression. Stimulation of whole blood with Ang II, a combination of IL6, IFN and TNFα (CytMix) or a combination (Ang+CytMix) for 4 h ex vivo at 37C did not affect AT1R in MONO or NEUTRO at baseline or high salt, but CytMix and CytMix+Ang increased AT1R during low salt. Interestingly, in NEUTRO, the AT2R displayed a decrease upon CytMix and CytMix+Ang, not dependent upon salt intake. Conclusions: MONO and NEUTRO express AT1R and AT2R. Low salt did not affect AT2R or AT1R expression. During low salt intake, MONO and NEUTRO stimulated with CytMix or CytMix+Ang displayed increased AT1R expression. This study shows that salt intake differentially affects AT1R and AT2R expression in leukocyte subtypes.

Dietary salt intake assessed by 24 h urinary sodium excretion in Australian schoolchildren aged 5-13 years.

To measure total daily salt intake using 24 h urinary Na excretion within a sample of Victorian schoolchildren aged 5-13 years and to assess discretionary salt use habits of children and parents. Cross-sectional study. Completed within a convenience sample of independent primary schools (n 9) located in Victoria, Australia. Two hundred and sixty children completed a 24 h urine collection over a school (34%) or non-school day (66%). Samples deemed incomplete (n 18), an over-collection (n 1) or that were incorrectly processed at the laboratory (n 3) were excluded. The sample comprised 120 boys and 118 girls with a mean age of 9.8 (SD 1.7) years. The average 24 h urinary Na excretion (n 238) was 103 (SD 43) mmol/24 h (salt equivalent 6.0 (SD 2.5) g/d). Daily Na excretion did not differ by sex; boys 105 (SD 46) mmol/24 h (salt equivalent 6.1 (SD 2.7) g/d) and girls 100 (SD 41) mmol/24 h (salt equivalent 5.9 (SD 2.4) g/d; P=0.38). Sixty-nine per cent of children (n 164) exceeded the recommended daily Upper Limit for Na. Reported discretionary salt use was common: two-thirds of parents reported adding salt during cooking and almost half of children reported adding salt at the table. The majority of children had salt intakes exceeding the recommended daily Upper Limit. Strategies to lower salt intake in children are urgently required, and should include product reformulation of lower-sodium food products combined with interventions targeting discretionary salt use within the home.

Low daily salt intake is correlated with albuminuria in patients with type 2 diabetes

Both high and low salt intakes have been reported to be associated with an increased risk of cardiovascular events. The aim of this study was to investigate the relationship between daily salt intake and albuminuria, a marker of diabetic nephropathy and cardiovascular disease, in patients with type 2 diabetes. We classified 270 patients with type 2 diabetes, who were not receiving antihypertensive medication into four groups according to their daily salt intake (<8, 8-10, 10-12 and >12 g per day). We investigated the relationship between daily salt intake and the logarithm of urinary albumin excretion (UAE). A multivariate linear regression analysis was used to evaluate whether daily salt intake independently correlated with the logarithm of UAE. In addition, we assessed the contribution of the variables, including age, sex, duration of diabetes, body mass index, systolic blood pressure, hemoglobin A(1C), low-density lipoprotein cholesterol, triglycerides, serum creatinine, alcohol intake, smoking status and square of (daily salt intake-10) on albuminuria, defined as a UAE>30 mg g(-1) of creatinine, using a multiple logistic regression analysis. The logarithm of the UAE was lowest in the third quartile of daily salt intake. The multivariate linear regression analysis demonstrated that the logarithm of the UAE was significantly correlated with the quadratic term of daily salt intake centered at 10 g per day (β=0.170, P=0.008). The multivariate logistic regression analysis demonstrated that the odds ratio (95% confidence interval) of albuminuria was 3.996 (1.295-12.327; P=0.016) in patients whose daily salt intake was less than 8 g per day compared with patients whose daily salt intake was 10-12 g per day. In conclusion, low daily salt intake was correlated with albuminuria in patients with type 2 diabetes, who were not receiving antihypertensive medication.

Relationship between achieved blood pressure, dietary habits and cardiovascular disease in hypertensive patients treated with olmesartan: the OMEGA study

We investigated the relationship between cardiovascular disease (CVD) and the achieved blood pressure, dietary habits and the presence/absence of metabolic syndrome (MetS) in hypertensive patients treated with olmesartan medoxomil. A prospective cohort study with a 3-year follow-up was conducted in 14 721 olmesartan-naive outpatients (mean age: 64.9 years, 49.6% women) with essential hypertension. The association of CVD with achieved blood pressure, dietary habits and MetS was investigated by Cox proportional hazards analysis. There were 3059 patients (31.8%) with MetS (Japanese criteria) among 9625 evaluable patients. The mean baseline blood pressure was 157.4/88.8 mm Hg, which decreased to 134.0/76.1 mm Hg during treatment (P<0.0001). The annual incidence of CVD was 7.15 per 1000 persons during the study period. When the achieved blood pressure was stratified according to the Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2009), the risk of CVD increased significantly along with the severity of hypertension (P<0.0001), especially the risk of stroke. Investigation of dietary habits revealed a significant association between salt intake and the risk of stroke. Higher salt intake was associated with a significantly higher risk of stroke than lower salt intake (hazard ratio, 1.897; 95% confidence interval, 1.003–3.590). Blood pressure was well controlled in both patients with and without MetS, and there was no significant difference in the incidence of events between the two groups. In conclusion, the severity of hypertension (achieved blood pressure) is associated with the incidence of CVD, and the results of this study suggest that tight blood pressure control and salt restriction are important for preventing stroke.

Loss of renal medullary endothelin B receptor function during salt deprivation is regulated by angiotensin II

We have recently demonstrated that chronic infusion of exogenous ANG II, which induces blood pressure elevation, attenuates renal medullary endothelin B (ET(B)) receptor function in rats. Moreover, this was associated with a reduction of ET(B) receptor expression in the renal inner medulla. The aim of this present work was to investigate the effect of a physiological increase in endogenous ANG II (low-salt diet) on the renal ET system, including ET(B) receptor function. We hypothesized that endogenous ANG II reduces renal medullary ET(B) receptor function during low-salt intake. Rats were placed on a low-salt diet (0.01-0.02% NaCl) for 2 wk to allow an increase in endogenous ANG II. In rats on normal-salt chow, the stimulation of renal medullary ET(B) receptor by ET(B) receptor agonist sarafotoxin 6c (S6c) causes an increase in water (3.6 ± 0.4 from baseline vs. 10.5 ± 1.3 μl/min following S6c infusion; P < 0.05) and sodium excretion (0.38 ± 0.06 vs. 1.23 ± 0.17 μmol/min; P < 0.05). The low-salt diet reduced the ET(B)-dependent diuresis (4.5 ± 0.5 vs. 6.1 ± 0.9 μl/min) and natriuresis (0.40 ± 0.11 vs. 0.46 ± 0.12 μmol/min) in response to acute intramedullary infusion of S6c. Chronic treatment with candesartan restored renal medullary ET(B) receptor function; urine flow was 7.1 ± 0.9 vs. 15.9 ± 1.7 μl/min (P < 0.05), and sodium excretion was 0.4 ± 0.1 vs. 1.1 ± 0.1 μmol/min (P < 0.05) before and after intramedullary S6c infusion, respectively. Receptor binding assays determined that the sodium-depleted diet resulted in a similar level of ET(B) receptor binding in renal inner medulla compared with rats on a normal-salt diet. Candesartan reduced renal inner medullary ET(B) receptor binding (1,414 ± 95 vs. 862 ± 50 fmol/mg; P < 0.05). We conclude that endogenous ANG II attenuates renal medullary ET(B) receptor function to conserve sodium during salt deprivation independently of receptor expression.

High salt intake in pregnancy alters maturation of glomeruli in the rat offspring

There is currently discussion on the optimal salt intake and uncertainty whether both high and low salt intake is associated with adverse effects. One aspect has so far not be considered, i.e. the potential impact of salt intake during pregnancy on kidney function and blood pressure in the offspring. Faulty fetal programming, amongst others by high or low salt intake, leads to alterations in kidney morphology and albuminuria in the offspring. A low number of glomeruli is known to cause high blood pressure later in life. It was the purpose of the present study to clarify whether very high (or low) salt intakes in pregnancy affect kidney development in the offspring. Sprague-Dawley rats were fed normal (0.15%), medium (1.3%), or high (8.0%) salt diet during pregnancy and weaning. The number of glomeruli (mature, immature, and S-shape bodies) was assessed at 1 week postnatally. The expression of proteins of interest was assessed (by western blotting) at 1 week postnatally and at term. There was no difference between the groups with respect to litter size, birth weight, and placenta size. At age 1 week the number of S-shaped bodies was significantly lower (405±308) and the number of mature glomeruli (818±405) and layers of developing glomeruli (7.1±0.6) was significantly higher in the offspring of mothers on high-salt compared to the medium or low salt groups (1044±490, 460±304, and 5.9±0.9 respectively). As a net result the total number of glomeruli was significantly lower in the offspring of mothers on high-salt (9476±1264) compared to the medium or low salt groups (11175±1920). At 1 week of age in the offspring of mothers on high salt the glomeruli were bigger compared to lower salt intake. The expression of Pax-2 (54±23% vs. 100±28%) and FGF-2 (72±33% vs. 100±30%) was significantly lower in the offspring of mothers on high-salt consistent with their causative role. We conclude that high maternal salt intake during pregnancy accelerates maturation of glomeruli in the offspring, but reduces the final number of glomeruli.

Increased susceptibility to hypertensive renal disease in streptozotocin-treated diabetic rats is not modulated by salt intake

In early type 1 diabetes mellitus, renal salt handling is dysregulated, so that the glomerular filtration rate becomes inversely proportional to salt intake. The salt paradox occurs in both humans and rats and, with low salt intake, results in diabetic hyperfiltration. We tested whether increased salt intake could reduce the susceptibility to injury of non-clipped kidneys in diabetic rats with pre-existing Goldblatt hypertension. Male Long-Evans rats were made hypertensive and half were then made diabetic. Blood glucose was maintained at ~20-25 mmol/l by insulin implants. One half of each received only the salt in normal chow (1% by weight) and the other half received added salt in drinking water to equal 2.7% by weight of food intake. Weekly 24 h blood pressure records were acquired by telemetry during the 4-month experiment. Systolic blood pressure was not affected by diabetes or increased salt intake, alone or together. Autoregulation was highly efficient in the non-clipped kidney of both intact and diabetic rats. Histological examination showed minor injury in the clipped kidney, which did not differ among groups. The non-clipped kidney showed extensive pressure-dependent glomerular and vascular injury in both intact and diabetic rats. The relationship between pressure and injury was shifted toward lower blood pressure in diabetic rats, indicating that diabetes increased the susceptibility of the kidney to injury despite preservation of autoregulation. The increased susceptibility was not affected by high salt intake in the diabetic rats, thus disproving the hypothesis.

Mitochondria function and structure in brown adipose tissue is influenced by maternal low salt intake during the perinatal period

ObjectiveTo evaluate brown adipose tissue (BAT) structure and function in female offspring of dams fed low salt diet during the perinatal period.MethodsFemale Wistar rats were fed low (LS: 0.15%) or normal (NS: 1.3% NaCl) salt diet since 8 weeks of age. At 12 weeks of age they were mated. After weaning, all offspring, were fed standard chow. Body temperature (T) was measured during 24 hours in adult female offspring (oLS or oNS) exposed to a cold (C) or room temperature (RT) environment. Gene expression (GE) of uncoupling protein‐1 (UCP1). PPARγ (PP), PGC1α (PG) and FOX C2 (FO) and mitochondria surface area (MIT) by electron microscopy were analyzed in BAT. Serum coenzyme Q10 was measured by HPLC.Results(p&lt;0.05, n=5/group): Compared to RT, during day time, T was lower in both offspring groups exposed to C. During night time, T was lower only in oNS exposed to C. Compared to oNS, GE of UCP1, PP and FO were lower (20%, 19%, and 57%, respectively) in oLS exposed to RT but not to C. GE of UCP1 and PG were higher (24% and 43%, respectively) in oLS exposed to C than in oLS exposed to RT. MIT was higher (76%) in oNS exposed to C than oNS exposed to RT. Compared to RT, Q10 was higher (110%) in oNS and lower (53%) in oLS exposed to C.ConclusionsLow salt intake during the perinatal period is associated with alterations in the response to cold exposure and of gene expression of factors related to energy metabolism in the offspring.Supported by FAPESP.

Plasma sodium and blood pressure in individuals on haemodialysis

To study the relationship between pre-dialysis plasma sodium and blood pressure (BP), we performed an audit of patients who were on stable haemodialysis at St Bartholomew's and The Royal London Hospital from 1 June 2009 to 15 June 2010. There were 651 patients with 7445 dialysis sessions where both plasma biochemistry and BP were measured before haemodialysis. We found a significant association between plasma sodium and both systolic and diastolic BP. A 1 mmol l(-1) increase in plasma sodium was related to 0.65/0.36 mm Hg increase in BP (P<0.001 for both systolic and diastolic BP) after adjusting for potential confounding factors, including weight gain between dialyses and plasma albumin, both of which are crude indices of extracellular fluid volume. A separate analysis excluding individuals who were on BP treatment showed a similar relationship, with a 1-mmol l(-1) increase in plasma sodium associated with 0.82/0.56 mm Hg increase in BP (P<0.001 for both, N=177). These results provide further support for the accumulating evidence that plasma sodium has an important role in regulating BP, which may be independent of extracellular volume. Our findings in conjunction with other evidence suggest that small changes in plasma sodium could be an important mechanism for the beneficial effects of lower dialysate sodium and lower salt intake on BP in haemodialysis patients.

Angiotensin II- and Salt-Induced Kidney Injury through Rac1-Mediated Mineralocorticoid Receptor Activation

Experiments with hyperaldosteronemic animals suggest that, despite lowering plasma aldosterone, salt worsens renal injury by paradoxical activation of the mineralocorticoid receptor (MR). Salt and aldosterone synergistically contribute to renal impairment through Rac1-mediated activation of the MR, but whether angiotensin II also promotes renal injury through this mechanism is unknown. Here, we placed angiotensin II-overproducing double transgenic Tsukuba hypertensive mice on a low- or high-salt intake for 6 weeks and treated some animals with adrenalectomy, the MR antagonist eplerenone, the Rac inhibitor EHT1864, or hydralazine. High-salt intake, but not low-salt intake, led to hypertension and prominent kidney injury. Adrenalectomy prevented angiotensin II/salt-induced nephropathy in mice receiving high-salt intake, which was recapitulated by aldosterone supplementation, suggesting the involvement of aldosterone/MR signaling. Plasma aldosterone levels, however, were lower in high- than low-salt conditions. Instead, angiotensin II/salt-evoked MR activation associated with Rac1 activation and was not dependent on plasma aldosterone level. Both EHT1864 and eplerenone repressed the augmented MR signaling and mitigated kidney injury with partial but significant reduction in BP with high-salt intake. Hydralazine similarly reduced BP, but it neither suppressed the Rac1-MR pathway nor ameliorated the nephropathy. Taken together, these results show that angiotensin II and salt accelerate kidney injury through Rac1-mediated MR activation. Rac inhibition may be a promising strategy for the treatment of CKD.

Salt intake during pregnancy alters offspring’s myocardial structure

Background and AimTo evaluate the effects of low or high salt intake during pregnancy on left ventricle of adult male offspring. Methods and resultsLow- (LS, 0.15%), normal- (NS, 1.3%) or high-salt (HS, 8% NaCl) diet was given to Wistar rats during pregnancy. During lactation all dams received NS as well as the offspring after weaning. To evaluate cardiac response to salt overload, 50% of each offspring group was fed a high-salt (hs, 4% NaCl) diet from the 21st to the 36th week of age (LShs, NShs, HShs). The remaining 50% was maintained on NS (LSns, NSns and HSns). Echocardiography was done at 20 and 30 weeks of age. Mean blood pressure (MBP), histology and left ventricular angiotensin II content (AII) were analyzed at 36 weeks of age. Interventricular septum, left ventricular posterior wall and relative wall thickness increased from the 20th to the 30th week of age only in HShs, cardiomyocyte mean volume was higher in HShs compared to NShs, LShs and HSns. AII and left ventricular fibrosis were not different among groups. ConclusionsHS during pregnancy programs adult male offspring to a blood pressure and angiotensin II independent concentric left ventricular hypertrophy, with no fibrosis, in response to a chronic high-salt intake.

Role of blood pressure in mediating the influence of salt intake on renin expression in the kidney

The salt intake of an organism controls the number of renin-producing cells in the kidney by yet undefined mechanisms. This study aimed to assess a possible mediator role of preglomerular blood pressure in the control of renin expression by oral salt intake. We used wild-type (WT) mice and mice lacking angiotensin II type 1a receptors (AT(1a)-/-) displaying an enhanced salt sensitivity to renin expression. In WT kidneys, we found renin-expressing cells at the ends of all afferent arterioles. A low-salt diet (0.02%) led to a moderate twofold increase in renin-expressing cells along afferent arterioles. In AT(1a)-/- mice, lowering of salt content led to a 12-fold increase in renin expression. Here, the renin-expressing cells were distributed along the preglomerular vascular tree in a typical distal-to-proximal distribution gradient which was most prominent at high salt intake and was obliterated at low salt intake by the appearance of renin-expressing cells in proximal parts of the preglomerular vasculature. While lowering of salt intake produced only a small drop in blood pressure in WT mice, the marked reduction of systolic blood pressure in AT(1a)-/- mice was accompanied by the disappearance of the distribution gradient from afferent arterioles to arcuate arteries. Unilateral renal artery stenosis in AT(1a)-/- mice on a normal salt intake produced a similar distribution pattern of renin-expressing cells as did low salt intake. Conversely, increasing blood pressure by administration of the NOS inhibitor N-nitro-l-arginine methyl ester or of the adrenergic agonist phenylephrine in AT(1a)-/- mice kept on low salt intake produced a similar distribution pattern of renin-producing cells as did normal salt intake alone. These findings suggest that changes in preglomerular blood pressure may be an important mediator of the influence of salt intake on the number and distribution of renin-producing cells in the kidney.

Second morning urine method is superior to the casual urine method for estimating daily salt intake in patients with hypertension

The accuracy of the casual urine (CU) method for estimating daily salt intake was compared with the second morning urine (SMU) method and with 24-h urine collection (24 UC) method as the gold standard. Data were obtained from three previously reported studies, in which we evaluated the daily salt intake by the SMU method. Using SMU samples from 1315 outpatients, the estimated salt intake was lower with the CU method than the SMU method. In inpatients with a daily salt intake of 7, 8 or 18 g, the CU method was applied to SMU specimens. It underestimated salt intake compared with the 24-h collection method whereas the SMU method and 24 UC method gave similar results. In the present study, 24 UC was done and then urine was collected at 0800, 1100, 1400, 1700 and 1900 hours, with a daily salt intake of 6 g in 8 inpatients, 10 g in 11 inpatients or 15 g in 5 inpatients. In comparison with the 24 UC method, the CU method underestimated a high salt intake (15 g) when morning specimens were used and overestimated a low salt intake (6 g) when afternoon specimens were used. The correlation between the CU method and 24 UC method was weaker (R = 0.57) than that between the SMU method and 24 UC method (R = 0.85). In conclusion, the CU method is heavily influenced by the timing of urine collection and by the actual daily salt intake, so the SMU method provides a better estimate of individual salt intake.

Association between Habitual Dietary Salt Intake and Risk of Gastric Cancer: A Systematic Review of Observational Studies

Purpose. Systematic reviews of case-control and prospective studies showed a positive association between habitual salt intake and gastric cancer. Given new studies published thereafter, we carried out a meta-analysis to assess the association between dietary salt intake and gastric cancer. Methods. Case-control studies and cohort studies published between January 1992 and January 2012 on PubMed and Embase were searched. We quantified associations between salt intake and gastric cancer with meta-analysis. Results. Eleven studies (7 case controls and 4 cohorts) finally were included in the meta-analysis (total population: n = 2076498; events: n = 12039). The combined odds ratio showed significantly positive association between high salt intake and gastric cancer compared with low salt intake (OR = 2.05, 95% CI [1.60, 2.62]; P < 0.00001). In subgroup meta-analysis, findings were slightly different when analyses were restricted to salty food intake (OR = 2.41, 95% CI [2.08, 2.78]; P < 0.00001) as well as in Asia (OR = 1.27 95% CI [1.22, 1.32]; P < 0.00001). There was no evidence that sample size, exposure assessment substantially influenced the estimate of effects. Conclusions. The systemic review supports the hypothesis that dietary salt intake is positively associated with the risk of gastric cancer.

Target Organ Damage in Hypertension

Target Organ Damage in Hypertension

How Can Diet Influence the Risk of Stroke?

Cerebrovascular diseases are the second cause of mortality in the world, and hypertension is considered a main risk factor for occurrence of stroke. The mechanisms responsible for the increased stroke risk remain unclear. However, dietary interventions have been applied in the management and treatment of their risk factors, which include increased blood pressure levels, obesity, diabetes, and dyslipidemia. Further studies should be conducted to assess the effects of carotenoids, flavonoids, n-3 polyunsaturated fats, and lower salt and high glycemic index intake in risk of stroke.

Salt and Hypertension: An Evolutionary Perspective

Despite overwhelming evidence linking increased salt intake to hypertension, the relation is still disputed in some circles. Viewing the introduction of salt to human diet on an evolutionary time scale would help us better understand the role of salt in hypertension. Humans and related species evolved in a salt-free environment over millions of years with intense evolutionary pressure for the selection of salt conserving genes. The recorded history confirms how rare and inaccessible salt has been until recently. Thrusting the species that has exquisitely adapted to very low salt intake into salt surfeit conditionsrepresents evolutionary mismatch with catastrophic health consequences. More than a quarter of human populations suffer from hypertension. World Health Organization (WHO) and many governments have now taken action to reduce dietary intake of salt in an effort to reduce the incidence of hypertension and the associated cardiovascular morbidity and mortality.

Effects of Benidipine Hydrochloride on Autonomic Nervous Activity in Hypertensive Patients with Highand Low-salt Diets

The effects of benidipine hydrochloride (CAS 91559-74-5, Coniel) on autonomic nervous activity in hypertensive patients with high- and low-salt diets were investigated. Six patients having a urinary sodium excretion of 80 mEq/day or less (low salt group) and 6 patients having a urinary sodium excretion of 200 mEq/day or more (high salt group) were orally given benidipine hydrochloride (4 mg). Before and four weeks after the treatment with benidipine, 24-h circadian variation in blood pressure and 24-h Holter electrocardiogram (ECG) were recorded. The low frequency power spectrum of heart rate (LF power; 0.04-0.15 Hz), high frequency power spectrum of heart rate (HF power; 0.15-0.40 Hz), and the ratio of LF to HF (LF/HF) were calculated, and these parameters were averaged every hour in every subject. HF power was significantly lower and LF/HF ratio was significantly higher in the high-salt group than in the low-salt group before the treatment. However, the benidipine treatment significantly increased the HF power in both groups, particularly in the high-salt group, and significantly decreased the LF/HF ratio in both groups. Moreover, there was no significant difference in the antihypertensive effect of benidipine between the high- and low-salt intake groups. These results suggest that benidipine favourably influences blood pressure and autonomic nervous activity in hypertensive patients with a high-salt intake. It is concluded that benidipine may be useful for improving the development of salt-induced hypertension and its accompanying haemodynamic responses.

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.

Reformulation of Romanian Meat Products and Cheeses: is this a Necessity for a Lower Salt Intake?

Reducing salt is a major task for companies all over the world. Scientific evidence has linked excessive salt consumption to increased risk of high blood pressure.&#x0D; The question we tried to answer to is if meat products and cheeses need to be reformulated, in order to bring down their salt content, taking in account the daily intake of cold cuts and diary products in our country. The intake was assessed by 7-days food diaries, completed by a representative sample of Romanians. The values used for the salt content were computed from data gathered in Romania since 2007. &#x0D; The average value of salt for Romanian cheeses is 2.4 g /100 g and for meat products, 2, 2 g /100 g. The food diaries showed that meat products and cheeses cover low percents of the daily salt intake (4%; 4%), with little variations between regions of the country. The present study concludes that cheeses and cold cuts, although consumed in all Romanian regions, have not a great contribution to the total salt intake in our country, so reformulation is not an emergency. However, the producers have to target in future a better management of the use of salt in the food chains, in the frame of advised descendent trends of the salt quantity introduced in human food. It has to be kept in mind that as long as the technological process allows it, every milligram of salt taken away from the product `s recipe is a helper of the consumer `s health.