Colonic expression of calcium transporter TRPV6 is regulated by dietary sodium butyrate.

Dietary fibers have been shown to increase the intestinal absorption of calcium (Ca2+) and magnesium (Mg2+). However, the mechanisms that explain the enhanced electrolyte absorption remain unknown. Therefore, this study aims to investigate the short-term and long-term effects of 5% (w/w) sodium butyrate (Na-butyrate), an important end-metabolite of bacterial fermentation of dietary fibers, on Ca2+ and Mg2+ homeostasis in mice. Serum Ca2+ levels were only significantly increased in mice treated with Na-butyrate for 1 day. This was associated with a twofold increase in the mRNA expression levels of Trpv6 in the proximal and distal colon. Contrary, Na-butyrate did not affect serum Mg2+ concentrations at either of the intervention periods. However, we observed a reduction in urinary Mg2+ excretion, although not significantly, after 1 day of treatment. A significant reduction of 2.5-fold in urinary Mg2+ excretion was observed after 14 days of treatment. Indeed, 14-day Na-butyrate supplementation increased colonic Trpm7 expression by 1.2-fold compared to control mice. In conclusion, short-term Na-butyrate supplementation increases serum Ca2+ levels in mice. This was associated with increased mRNA expression levels of Trpv6 in the colon, suggesting that Na-butyrate regulates the expression of genes involved in active intestinal Ca2+ absorption.

Dietary sodium butyrate ameliorated the blood stress biomarkers, heat shock proteins, and immune response of Nile tilapia (Oreochromis niloticus) exposed to heat stress.

The present study investigated the effects of sodium butyrate (SB) on the growth performance, histomorphology, immune response, and stress related markers of Nile tilapia subjected to heat stress. SB was incorporated at 0, 0.5, 1, 1.5, and 2 g per kg diet and fed to fish for 8 weeks. The obtained results revealed significantly improved growth performance with a decreased feed conversion ratio in the fish fed SB (P < 0.05). In the anterior, middle, and distal parts of the intestine, villus length and width and internal villi distance as well as the number of goblet cells were increased in the fish fed SB (P < 0.05). The blood total protein, hemoglobin, and white and red blood cell counts showed a significant quadratic influence (P < 0.05). The survival rate for Nile tilapia exposed to heat stress for 48 h revealed that the SB fed groups had noticeably higher survival rates. Dietary SB significantly increased the phagocytic index and lysozyme and phagocytic activities both before and after heat stress (P < 0.05). After heat stress, blood glucose decreased significantly with SB feeding at 0.5, 1, or 1.5 g per kg diet, while cortisol was reduced in fish fed 1.5 or 2 g per kg diet (P < 0.05). Additionally, in fish fed SB, superoxide dismutase (SOD), catalase, and glutathione peroxidase activities were significantly increased both before and after heat stress, while malondialdehyde was decreased by SB feeding (P < 0.05). Liver heat shock protein 70 and SOD gene expression were significantly upregulated in fish fed on SB at 1 g per kg diet (P < 0.05). Thus, supplementation with SB at 1-2 g per kg diet can be used effectively in tilapia diets for improving growth, feed efficiency, and immune response as well as for tolerance to heat stress.

Effects of two new formulas of dietary buffers with a high buffering capacity containing Na or K on performance and metabolism of mid-lactation dairy cows.

The present study was conducted to evaluate the effect of two new formulas of dietary buffers on intake, total tract digestibility, rumen pH, blood metabolites, and milk production of mid-lactation dairy cows. Nine multiparous cows (594 ± 46 kg BW; mean ± SD) averaging 120 ± 28 days in milk and producing 46.6 ± 3.4 kg/d were randomly assigned to a triplicate 3 × 3 Latin square. During each 21-d period, cows were offered one of three total mixed rations that varied in dietary buffer. The three types of dietary buffer were 1) 11.2 g/kg of dietary dry matter (DM) sodium bicarbonate (SB; control), 2) 8.7 g/kg of dietary DM high buffering capacity formula contained Na (HBNa), and 3) 7.4 g/kg of dietary DM high buffering capacity formula contained K (HBK). Each period was comprised of 14 d of dietary adaptation followed by 7 d of sampling. Measured buffering capacity was 102, 150 and 137 percent of NaHCO3 for SB, HBNa and HBK, respectively. The amount of Na and K were 270 and 0, 310 and 0, and 250 and 60 g/kg for SB, HBNa, and HBK, respectively. Dry matter intake (DMI) tended (P = 0.06) to be lower with HBK (20.6 kg/d) than SB (21.0 kg/d) and HBNa (21.2 kg/d). No treatment effects were observed on rumen pH (averaged 5.88) and DM digestibility in the total digestive tract (averaged 79.4%). Yields of actual milk (38.1 kg/d) and 3.5% fat corrected milk (31.6 kg/d) were not affected by treatments, whereas yields of solid corrected milk (P = 0.07) and milk fat (P = 0.10) tended to be greater with HBK than SB and HBNa. Milk fat concentration in cows fed HBK was greater than in cows fed other treatments (32.5 vs. 29.5 and 29.6 g/kg; P = 0.04). Concentration of milk protein (32.2 vs. 30.6 g/kg) and lactose (46.8 vs. 44.4 g/kg) also were greater in cows fed HBK than those fed SB (P = 0.02). Efficiency of milk production was greater in cows fed HBK than SB (1.86 vs. 1.80; P = 0.01), whereas efficiency of solid corrected milk production was greater in HBK than SB and HBNa (1.64 vs. 1.51 and 151; P = 0.02). Blood concentration of Ca was higher with HBK compared with SB and HBNa (10.4 vs. 9.7 and 9.9 mg/dL, respectively; P = 0.01). These results indicated that under the current experimental condition, supplementation of dairy cow diet with a high buffering capacity buffer containing 60 g/kg K decreased DMI and improved milk composition and milk efficiency of mid-lactation dairy cows.

The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions.

Pentraxin-3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt-induced hypertension. We investigated the responses of pentraxin-3 to sodium and potassium supplementation to elucidate the potential role of pentraxin-3 in salt-induced hypertension. A total of 48 participants from northwest China were enrolled. All participants were maintained on a 3-day normal diet, which was sequentially followed by a 7-day low-sodium diet, a 7-day high-sodium diet, and a 7-day high-sodium plus potassium diet. Plasma concentrations of pentraxin-3 were assessed using ELISA. Plasma pentraxin-3 decreased significantly during the low-salt period compared to baseline (0.57 ± 0.19 ng/mL vs 0.72 ± 0.33 ng/mL, P = .012) and increased during the high-salt period (0.68 ± 0.26 ng/mL vs 0.57 ± 0.19 ng/mL, P = .037). Potassium supplementation inhibited salt-induced increase in pentraxin-3 (0.56 ± 0.21 ng/mL vs 0.68 ± 0.26 ng/mL, P = .015). Ln-transformed pentraxin-3 at baseline was inversely correlated with BMI (r = -.349, P = .02), DBP (r = -.414, P = .005), MAP (r = -.360, P = .017). We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-hour urinary sodium during low and high Na+ periods (r = .269, P = .012) and a negative relationship with 24 hours urinary potassium excretion during high-salt and high-salt plus potassium periods (r = -.246, P = .02). These correlations remained significant after adjusting for confounders. Pentraxin-3 responses were more prominent in salt-sensitive individuals than salt-resistant individuals. Dietary salt and potassium interventions significantly altered circulating pentraxin-3.

Effects of dietary sodium on metabolites: the Dietary Approaches to Stop Hypertension (DASH)-Sodium Feeding Study.

Background: High sodium intake is known to increase blood pressure and is difficult to measure in epidemiologic studies.Objective: We examined the effect of sodium intake on metabolites within the DASH (Dietary Approaches to Stop Hypertension Trial)-Sodium Trial to further our understanding of the biological effects of sodium intake beyond blood pressure.Design: The DASH-Sodium Trial randomly assigned individuals to either the DASH diet (low in fat and high in protein, low-fat dairy, and fruits and vegetables) or a control diet for 12 wk. Participants within each diet arm received, in random order, diets containing high (150 nmol or 3450 mg), medium (100 nmol or 2300 mg), and low (50 nmol or 1150 mg) amounts of sodium for 30 d (crossover design). Fasting blood samples were collected at the end of each sodium intervention. We measured 531 identified plasma metabolites in 73 participants at the end of their high- and low-sodium interventions and in 46 participants at the end of their high- and medium-sodium interventions (N = 119). We used linear mixed-effects regression to model the relation between each log-transformed metabolite and sodium intake. We also combined the resulting P values with Fisher's method to estimate the association between sodium intake and 38 metabolic pathways or groups.Results: Six pathways were associated with sodium intake at a Bonferroni-corrected threshold of 0.0013 (e.g., fatty acid, food component or plant, benzoate, γ-glutamyl amino acid, methionine, and tryptophan). Although 82 metabolites were associated with sodium intake at a false discovery rate ≤0.10, only 4-ethylphenylsufate, a xenobiotic related to benzoate metabolism, was significant at a Bonferroni-corrected threshold (P < 10-5). Adjustment for coinciding change in blood pressure did not substantively alter the association for the top-ranked metabolites.Conclusion: Sodium intake is associated with changes in circulating metabolites, including gut microbial, tryptophan, plant component, and γ-glutamyl amino acid-related metabolites. This trial was registered at clinicaltrials.gov as NCT00000608.

Associations of Usual 24-Hour Sodium and Potassium Intakes with Blood Pressure and Risk of Hypertension among Adults in China's Shandong and Jiangsu Provinces.

BACKGROUND/AIMS: High sodium intake and low intake of potassium can increase blood pressure (BP) and risk of developing hypertension. Few studies have examined the association between 24-h urinary sodium and potassium excretion and BP or risk of hypertension in China, and most used only a single 24-h urinary sample. METHODS: We analyzed data on 2281 participants aged 18-69 years by using two 24-h urinary sodium and potassium excretions from the supplemental baseline survey of the Shandong-Ministry of Health Action on Salt Reduction and Hypertension (SMASH) project. We used measurement error models to estimate usual intakes, multivariable linear regression to assess their association with B P, and logistic regression to estimate the risk of hypertension. RESULTS: The average usual intakes of sodium and potassium, and the mean sodium-potassium ratio, were 166.9 mmol/day, 25.3 mmol/day, and 6.8, respectively. All three measures were significantly associated with systolic BP (SBP) and diastolic BP (DBP), with an increase of 1.39 mmHg (95% confidence interval [CI] 0.44─2.34) in SBP and 0.94 mmHg (95% CI 0.34─1.55) in DBP for a 1-standard deviation (SD) (25.6mmol/day) increase in sodium intake, a decrease of 1.42 mmHg (95% CI -2.37─ -0.47) in SBP and 0.91 mmHg (95% CI -1.52─ -0.30) in DBP for a 1-SD (3.4 mmol/day) increase in potassium intake, and an increase of 0.97 mmHg (95% CI 0.36─1.58) in SBP and of 0.65 mmHg (95% CI 0.26─1.04) in DBP per unit increase in the sodium-to-potassium ratio. The adjusted odds ratios comparing the risk of hypertension among adults in the highest with those in the lowest quintile differ significantly for potassium (0.51; 95% CI 0.29─0.88) and sodium-to-potassium ratio (1.40; 95% CI 1.01─1.94). CONCLUSIONS: Our results suggested that higher sodium and lower potassium intakes are associated with increased BP and risk of hypertension in the Shandong and Jiangsu adults.

Modulation of antioxidant defense and immune response in zebra fish (Danio rerio) using dietary sodium propionate.

The present study explores the effect of dietary sodium propionate on mucosal immune response and expression of antioxidant enzyme genes in zebra fish (Danio rerio). Six hundred healthy zebra fish (0.42 ± 0.06 g) supplied, randomly stocked in 12 aquariums and fed on basal diets supplemented with different levels of sodium propionate [0 (control), 5, 10 and 20 g kg-1] for 8 weeks. At the end of the feeding trial, mucosal immune parameters (TNF-α, IL-1ß, Lyz), antioxidant enzyme (SOD, CAT) as well as heat shock protein 70 (HSP70) gene expression were measured. The results revealed feeding on sodium propionate significantly up-regulated inflammatory response genes (TNF-α, IL-1ß, Lyz) in a dose-dependent manner (P < 0.05). However, antioxidant enzyme genes significantly down-regulated in the treated group compared with control (P < 0.05). Also, HSP70 gene expression was higher in the liver of fish fed the basal diet and deceased with elevation of sodium propionate levels in the diet. These results showed beneficial effects of dietary sodium propionate on mucosal immune response as well as the antioxidant defense of zebra fish.

Electrolyte supplementation during severe energy restriction increases exercise capacity in the heat.

PURPOSE: This study examined the effects of sodium chloride and potassium chloride supplementation during 48-h severe energy restriction on exercise capacity in the heat. METHODS: Nine males completed three 48-h trials: adequate energy intake (100 % requirement), adequate electrolyte intake (CON); restricted energy intake (33 % requirement), adequate electrolyte intake (ER-E); and restricted energy intake (33 % requirement), restricted electrolyte intake (ER-P). At 48 h, cycling exercise capacity at 60 % VO2 peak was determined in the heat (35.2 °C; 61.5 % relative humidity). RESULTS: Body mass loss during the 48 h was greater during ER-P [2.16 (0.36) kg] than ER-E [1.43 (0.47) kg; P < 0.01] and CON [0.39 (0.68) kg; P < 0.001], as well as greater during ER-E than CON (P < 0.01). Plasma volume decreased during ER-P (P < 0.001), but not ER-E or CON. Exercise capacity was greater during CON [73.6 (13.5) min] and ER-E [67.0 (17.2) min] than ER-P [56.5 (13.1) min; P < 0.01], but was not different between CON and ER-E (P = 0.237). Heart rate during exercise was lower during CON and ER-E than ER-P (P < 0.05). CONCLUSIONS: These results demonstrate that supplementation of sodium chloride and potassium chloride during energy restriction attenuated the reduction in exercise capacity that occurred with energy restriction alone. Supplementation maintained plasma volume at pre-trial levels and consequently prevented the increased heart rate observed with energy restriction alone. These results suggest that water and electrolyte imbalances associated with dietary energy and electrolyte restriction might contribute to reduced exercise capacity in the heat.

Common Variants in Serum/Glucocorticoid Regulated Kinase 1 (SGK1) and Blood Pressure Responses to Dietary Sodium or Potassium Interventions: A family-Based Association Study.

BACKGROUND/AIMS: Serum/Glucocorticoid Regulated Kinase 1 (SGK1) plays a significant role in regulating renal Na(+) reabsorption, K(+) secretion, and blood pressure (BP). This study aimed to assess the association of common genetic variants in the SGK1 gene with BP responses to controlled dietary sodium or potassium interventions. METHODS: A total of 334 subjects from 124 families were recruited from the rural areas of northern China. After a three-day baseline observation, they were sequentially maintained a seven-day low-sodium diet (3g/day of NaCl or 51.3 mmol/day of sodium), a seven-day high-sodium diet (18 g/day of NaCl or 307.8 mmol/day of sodium) and a seven-day high-sodium plus potassium supplementation intervention (4.5 g/day of KCl or 60 mmol/day of potassium). Six single-nucleotide polymorphisms (SNPs) in the SGK1 gene were selected. RESULTS: After adjustment for multiple testing, SNP rs9376026 was significantly associated with diastolic BP (DBP) and mean arterial pressure (MAP) responses to low-sodium intervention (P = 0.018 and 0.022, respectively). However, the associations between selected SNPs in the SGK1 gene and BP responses to high-sodium or high-sodium plus potassium-supplementation intervention did not reach statistical significance. In addition, SNP rs9389154 and two other SNPs (rs1763509 and rs9376026) were associated respectively with systolic BP (SBP) and DBP at baseline (P = 0.040, 0.032, and 0.031, respectively). SNP rs3813344 was significantly associated with SBP, DBP, and MAP (P = 0.049, 0.015 and 0.018, respectively). CONCLUSION: Our study indicates that the genetic polymorphism in the SGK1 gene is significantly associated with BP responses to dietary sodium intervention.

Role of hypothalamic angiotensin type 1 receptors in pressure overload-induced mineralocorticoid receptor activation and salt-induced sympathoexcitation.

Pressure overload enhances salt-induced sympathoexcitation through hypothalamic mineralocorticoid receptor (MR)-epithelial Na channel activation. Pressure overload also increases hypothalamic angiotensin type 1 receptors (AT1R). However, the role of AT1R in pressure overload-induced MR activation and salt-induced sympathoexcitation remains unknown. Therefore, the aim of the present study was to address this question. We performed aortic banding (AB) on mice from the Institute of Cancer Research. The expression of hypothalamic MR, serum/glucocorticoid-induced protein kinase-1 (SGK-1) and AT1R increased independently of plasma renin activity at 2 or 4 weeks after AB. Next, we performed AB in AT1aR-knockout (KO) mice and c57BL6/J wild-type (WT) mice. Sham-operated (Sham) mice were used as a control. Four weeks after AB (AB-KO or AB-WT), the expression of hypothalamic MR and SGK-1 increased in both AB-WT and AB-KO compared with Sham-WT and Sham-KO, respectively. The expression of AT1R was also greater in AB-WT than in Sham-WT. In addition, mice were fed a high-salt (8%) diet for an additional 4 weeks (ABH-KO and ABH-WT). High salt loading increased the urinary excretion of norepinephrine, a marker of sympathetic activity in ABH-WT, concomitant with hypothalamic MR activation, but not in ABH-KO. These results indicate that pressure overload activated hypothalamic MR independently of AT1R. After salt intake, however, AT1R was necessary to maintain hypothalamic MR activation and salt-induced sympathoexcitation.

Effect of Flammulina velutipes on spent-hen breast meat tenderization.

An experiment was carried out to investigate the effects of powdered vegetable dip sauces to improve the tenderness of spent-hen breast meat. Our overall purpose was to find lower-priced materials for the tenderization of spent-hen breast meat. The spent-hen breast meat was dipped into vegetable powder for 24 h at 4°C, and then the samples were analyzed. In the results for vegetable-powder treated samples, those treated with papain and pineapple had higher (P ≤ 0.05) myofibrillar fragmentation indices compared with those of the other samples. The kiwi-, pineapple-, and Flammulina velutipes-powder (winter mushroom) treated samples had new peptides of about 32 kDa and degradation to 30 kDa. Also, the Flammulina velutipes-powder treated samples showed new peptides of 15 kDa. These data imply that Flammulina velutipes is superior for common use than papain or pineapple for the tenderization of spent-hen meat.

The influence of body mass index and renin-angiotensin-aldosterone system activity on the relationship between 25-hydroxyvitamin D and adiponectin in Caucasian men.

OBJECTIVE: Previous studies have suggested that circulating adiponectin concentrations are associated positively with vitamin D and negatively with body mass index (BMI) but have not accounted for the influence of the renin-angiotensin-aldosterone system (RAAS) in this relationship. This is particularly relevant because increased RAAS activity is associated with obesity and is known to lower adiponectin levels. We evaluated the association between adiponectin and 25-hydroxyvitamin D (25(OH)D) after controlling RAAS activity with dietary sodium equilibration and also evaluated whether this relationship was influenced by BMI. DESIGN: Cross-sectional study of 115 hypertensive Caucasian men from the Hypertensive Pathotype Consortium. METHODS: To manipulate RAAS activity, all subjects underwent 1 week of high dietary sodium (HS) diet to suppress RAAS and 1 week of low dietary sodium (LS) diet to stimulate RAAS. Linear regression was used to evaluate the association between adiponectin and 25(OH)D, and the effect of BMI on this relationship, in each dietary condition. RESULTS: Adiponectin was higher on HS, where circulating RAAS activity was low, when compared with LS (HS=2.9 versus LS=2.4 µg/ml, P<0.0001). 25(OH)D levels were positively associated with adiponectin, and BMI was a statistically significant effect modifier of the relationship between 25(OH)D and adiponectin on both diets (P interaction <0.01 between BMI and 25(OH)D). CONCLUSIONS: Higher 25(OH)D concentrations were independently associated with higher adiponectin levels, particularly when BMI was high. Dietary sodium balance and circulating RAAS activity did not appear to affect this relationship. Future studies should explore whether vitamin D supplementation increases adiponectin levels in obesity.

Effects of central sodium on epithelial sodium channels in rat brain.

We evaluated the effects of intracerebroventricular (icv) infusion of Na(+)-rich artificial cerebrospinal fluid (aCSF), with or without the mineralocorticoid receptor (MR) blocker spironolactone, on epithelial Na(+) channel (ENaC) subunits and regulators, such as MR, serum/glucocorticoid-inducible kinase 1, neural precursor cells expressed developmentally downregulated 4-like gene, 11beta-hydroxylase, and aldosterone synthase, in brain regions of Wistar rats. The effects of icv infusion of the amiloride analog benzamil on brain tissue and CSF Na(+) concentration ([Na(+)]) were also assessed. In the choroid plexus and ependyma of the anteroventral third ventricle, ENaC subunits are present in apical and basal membranes. Na(+)-rich aCSF increased beta-ENaC mRNA and immunoreactivity in the choroid plexus and increased alpha- and beta-ENaC immunoreactivities in the ependyma. Na(+)-rich aCSF increased alpha- and beta-ENaC-gold-labeled particles in the microvilli of the choroid plexus and in basolateral membranes of the ependyma. Spironolactone only prevented the increase in beta-ENaC immunoreactivity in the choroid plexus and ependyma. In the supraoptic nucleus, paraventricular nucleus, and subfornical organ, Na(+)-rich aCSF did not affect mRNA expression levels of the studied genes. Benzamil significantly increased CSF [Na(+)] in the control, but not Na(+)-rich, aCSF group. In contrast, benzamil prevented the increase in hypothalamic tissue [Na(+)] by Na(+)-rich aCSF. These results suggest that CSF Na(+) upregulates ENaC expression in the brain epithelia, but not in the neurons of hypothalamic nuclei. ENaC in the choroid plexus and ependyma appear to contribute to regulation of Na(+) homeostasis in the brain.

[Nutrition and hypertension: more than table salt]. / Alimentation et hypertension artérielle: au-delà du sel de table.

The role of dietary sodium intake in the development, and its impact on the treatment, of hypertension are well recognized. However, many other nutritional compounds have been shown, or are believed, to influence blood pressure. Some compounds, such as caffeine and fructose, may raise arterial blood pressure, whereas others might lower arterial blood pressure, for example garlic, dark chocolate, fibers and potassium. In this article, we review several alimentary compounds and their (hypothesized) mechanisms of action, as well as the available evidence supporting a role of these compounds in the "non pharmacological" treatment and prevention of hypertension.

Correlation between blood pressure responses to dietary sodium and potassium intervention in a Chinese population.

BACKGROUND: Blood pressure (BP) responses to dietary sodium and potassium intake vary among individuals. We examined the correlation between BP responses to dietary low-sodium, high-sodium, and potassium supplementation interventions in a feeding study. METHODS: A total of 1,906 Chinese aged > or = 16 years participated in the dietary intervention that included a 7-day low-salt intervention (51.3 mmol/day), a 7-day high-salt intervention (307.8 mmol/day), and a 7-day high-salt plus potassium supplementation (60 mmol/day) intervention. BP was measured nine times during the 3-day baseline observation and during the last 3 days of each intervention phase using a random-zero sphygmomanometer. RESULTS: The correlation coefficients (95% confidence intervals (CIs)) of the BP responses to low-sodium and high-sodium interventions were -0.47 (-0.51 to -0.44), -0.47 (-0.50 to -0.43), and -0.45 (-0.49 to -0.42) for systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP), respectively (all P < 0.0001). The correlation coefficients (95% CI) of the BP responses to high-sodium intervention and potassium supplementation were -0.52 (-0.56 to -0.49), -0.48 (-0.52 to 0.45), and -0.52 (-0.55 to -0.48) for SBP, DBP, and MAP, respectively (all P < 0.0001). The kappa coefficients were moderate, varying from 0.28 to 0.34, between BP responses to low-sodium and high-sodium interventions (all P < 0.0001). CONCLUSIONS: These results indicate there is a moderate correlation between BP responses to low-sodium and to high-sodium interventions, and BP responses to high-sodium intervention and potassium supplementation. Furthermore, our study suggests that individuals who were more sensitive to high-sodium diet might benefit more from a low-sodium and/or high-potassium intervention aimed at lowering BP levels.

The effects of high-impact and resistance exercise on urinary calcium excretion.

Although physical activity is known to improve bone mineralization, it is unclear whether this occurs through altered absorption and/or excretion. The purpose of this study was to investigate the effects of a high-impact and resistance-training exercise program versus a period of restricted physical activity on urinary calcium excretion. Ten healthy, moderately active men (27.0 +/- 5.8 yr) participated in a 3-wk randomized crossover study. Participants were assigned to complete either a period of daily participation in exercise including high-impact and resistance-training activities (EX) or a period of restriction in physical activity (NE) for 7 consecutive days. After a 1-wk washout period, participants completed the opposite trial. During both phases, participants consumed four 8-oz servings of low-fat (1%) milk daily and avoided other dietary and supplemental sources of calcium. Urine was collected throughout the final 72 hr of each study phase. Urinary calcium and sodium excretions were 14.7% +/- 17.1% and 15.8% +/- 9.9% lower (p < .05), respectively, during the EX phase than the NE phase. These results occurred despite participants consuming more (p < .05) sodium during the EX phase than the NE phase. These results suggest that healthy, moderately active men excrete significantly less urinary calcium concurrent with lower sodium excretion during a week of performing high-impact and resistance-training exercises versus a week of restricted physical activity. The reduction in urinary loss of calcium might be at least partially responsible for improved bone mineralization that has been observed during periods of greater physical activity.

Salt craving: the psychobiology of pathogenic sodium intake.

Ionic sodium, obtained from dietary sources usually in the form of sodium chloride (NaCl, common table salt) is essential to physiological function, and in humans salt is generally regarded as highly palatable. This marriage of pleasant taste and physiological utility might appear fortunate--an appealing taste helps to ensure that such a vital substance is ingested. However, the powerful mechanisms governing sodium retention and sodium balance are unfortunately best adapted for an environment in which few humans still exist. Our physiological and behavioral means for maintaining body sodium and fluid homeostasis evolved in hot climates where sources of dietary sodium were scarce. For many reasons, contemporary diets are high in salt and daily sodium intakes are excessive. High sodium consumption can have pathological consequences. Although there are a number of obstacles to limiting salt ingestion, high sodium intake, like smoking, is a modifiable behavioral risk factor for many cardiovascular diseases. This review discusses the psychobiological mechanisms that promote and maintain excessive dietary sodium intake. Of particular importance are experience-dependent processes including the sensitization of the neural systems underlying sodium appetite and the effects of sodium balance on hedonic state and mood. Accumulating evidence suggests that plasticity within the central nervous system as a result of experience with high salt intake, sodium depletion, or a chronic unresolved sodium appetite fosters enduring changes in sodium related appetitive and consummatory behaviors.

The in vivo effects of Tulbhagia violacea on blood pressure in a salt-sensitive rat model.

AIM OF THE STUDY: The in vivo effects of Tulbhagia violacea on systemic arterial blood pressure and on the renin-angiotensin system in a Dahl salt-sensitive rat model were investigated. MATERIALS AND METHODS: Animals were treated for 14 days intraperitoneally as follows: Tulbhagia violacea (Tvl) (50mg/kg b.w.), captopril (Cap) (10mg/kg b.w.) or DMSO (Con). Baseline blood pressures were recorded prior to the commencement of the study and biweekly during the experimental period. Urine volume and sodium concentration were measured during the experimental period. On day 15, animals were anaesthetized (sodium thiopentane, 50mg/kg, i.p.), blood samples for aldosterone levels were taken and the kidneys removed for determining AT1a mRNA expression. RESULTS: Cap and Tvl groups showed significantly reduced AT1a mRNA expressions by 3.11- and 5.03-fold, respectively, when compared to the Con group (p<0.05). When compared to baseline blood pressures (day 0); Cap and Tvl showed reductions in systolic blood pressure (SBP) of 7.76+/-0.41% and 9.12+/-0.31%, respectively (mean% decrease from day 0 to day 14). In contrast, in the Con group the systolic blood pressure increased from day 0 to day 14 by 4.66+/-0.56%. Blood pressure changes in all treated groups differed from Con significantly. Systolic blood pressure decreased with the decrease in AT1a mRNA expressions in these groups. When comparing day 0 to day 14, urine output increased in the Cap and Tvl groups. In the Con group, urinary volume was reduced by day 14 as compared to day 0. Urinary sodium excretion was increased in the treated groups by day 14. CONCLUSION: It can be concluded that Tulbhagia violacea reduces systemic arterial blood pressure in the Dahl rat by decreasing renal AT1 receptor gene expression and hence modulating sodium and water homeostasis.

Heritability of blood pressure responses to dietary sodium and potassium intake in a Chinese population.

The heritability of blood pressure responses to dietary intervention has not been well studied. We examined the heritability of blood pressure responses to dietary sodium and potassium intake in a family feeding study among 1906 study participants living in rural North China. The dietary intervention included a 7-day low-sodium feeding (51.3 mmol per day), a 7-day high-sodium feeding (307.8 mmol per day), and a 7-day high-sodium plus potassium supplementation (60 mmol per day). Blood pressure was measured 9 times during the 3-day baseline period preceding the intervention and also during the last 3 days of each intervention phase using a random-zero sphygmomanometer. Heritability was computed using maximum likelihood methods under a variance components model as implemented in the computer program SOLAR. The heritabilities of baseline blood pressure were 0.31 for systolic, 0.32 for diastolic, and 0.34 for mean arterial pressure. The heritabilities increased significantly under dietary intervention and were 0.49, 0.49, and 0.51 during low sodium; 0.47, 0.49, and 0.51 during high sodium; and 0.51, 0.52, and 0.53 during potassium supplementation for systolic, diastolic, and mean arterial pressure, respectively. The heritabilities for percentage of blood pressure responses to low sodium were 0.20, 0.21, and 0.23; to high-sodium were 0.22, 0.33, and 0.33; and to potassium supplementation were 0.24, 0.21, and 0.25 for systolic, diastolic, and mean arterial pressure, respectively. Our study indicated that the heritabilities of blood pressure under controlled dietary sodium and potassium intake were significantly higher than those under a usual diet. In addition, the heritabilities of blood pressure responses to dietary sodium and potassium intake were moderate in this study population.

Challenged sodium balance and expression of angiotensin type 1A receptor mRNA in the hypothalamus of Wistar and Dahl rat strains.

The present study investigates the influence of a chronic high Na+ diet (8% Na+) on the expression of the angiotensin type 1A (AT1A) receptor gene in the lamina terminalis and paraventricular nucleus of the hypothalamus (PVH) in normotensive Wistar (W) rats, as well as in Dahl salt-resistant (DR) and Dahl salt-sensitive (DS) rats. Three weeks of 8% Na+ diet led to a higher blood pressure in DS rats compared to DR and W rats. Moreover, the high Na+ diet was correlated with a decreased expression of AT1A receptor mRNA in the median preoptic nucleus (MnPO) and in the PVH of DS rats, compared to DR and W rats. Contrastingly, the AT1A receptor mRNA expression was not altered by the high Na+ diet in the forebrain circumventricular organs of all the rat strains. Interestingly, a furosemide-induced Na+ depletion was correlated with an increased expression of AT1A receptor mRNA in the PVH, MnPO and SFO of both the DS and DR rats. It is concluded that chronic high Na+ diet did differently regulate the expression of AT1A receptor mRNA in two hypothalamic integrative centers for hydromineral and cardiovascular balance (the PVH and MnPO) in DS rats, compared to DR and W rats. However, the AT1A receptor mRNA expression was similarly regulated in DS and DR rats in response to an acute Na+ depletion, suggesting a distinct high Na+ -induced regulation of the AT1A receptor gene in the PVH and MnPO of DS rats.