High Sodium Group Research Articles

Abstract P397: Effects of Dietary Sodium Reduction on Systemic Inflammation: Findings from DASH-Sodium Study

Background: High sodium intake is a significant risk factor for hypertension and cardiovascular disease. Animal studies have demonstrated that high salt diet promotes tissue inflammation and increases systemic inflammation, such that it is plausible that sodium induced inflammation might be another pathway to hypertension. However, whether the link between dietary sodium intake and systematic inflammation in humans remains unclear due to limited human studies, different designs and inconsistent findings. Therefore, we tested the hypothesis that dietary sodium reduction reduces systemic inflammation in humans by leveraging the randomized controlled trial design of the DASH-Sodium study. Methods: DASH-Sodium study was a multicenter, randomized trial comparing the effects on blood pressure (BP) of three levels of sodium intake (3450 mg/d, 2300mg/d, and 1150 mg/d) in two diets (DASH vs American) among US adults. Five systematic inflammatory markers including hs-CRP, IFN-γ, IL-6, IL-10, and TNF-α were measured at each study visit in stored plasma samples from 224 participants. Two-level mixed-effects linear regression models were used to assess the effect of sodium reduction on inflammatory markers with adjustment of covariates. Results: A total of 224 participants (aged 49.4±9.5 yrs, 61% female, 62% black, and 2% other races) from the DASH-Sodium study were included in the analyses. Overall, compared to high sodium group, low sodium group had slightly elevated hs-CRP ( p =0.013), and intermediate sodium group had decreased TNF-α ( p =0.011). Both significances, however, disappeared after adjusting for multiple testing ( p adjust >0.01). Conclusion: Modest dietary sodium reduction as recommended did not induce significant changes in systematic inflammation in humans.

Calcium- and Sodium-Rich Food Intake among Koreans with and without Metabolic Syndrome: Cross-Sectional Analysis of the Korean Genome and Epidemiology Study.

The prevalence of metabolic syndrome (MetS) is increasing. While calcium and sodium are known nutritional factors used for managing MetS, few studies have focused on food-based analyses. This cross-sectional study examined the distribution of calcium- and sodium-rich food intake among Koreans with MetS. This cross-sectional analysis evaluated 130,423 participants from the Health Examinees-Gem cohort study. Foods contributing up to 90% of the calcium and sodium intake were selected from the semi-quantitative food frequency questionnaire, and consumption levels were calculated. MetS was defined as satisfying three or more criteria from the National Cholesterol Education Program Adult Treatment Panel III. The results are presented as odds ratios (OR) with an interquartile range (ORIQR) and 95% confidence interval. Participants with MetS showed a low calcium intake (ORIQR = 0.95 and 0.92 for men and women, respectively), low consumption of dairy products (ORIQR = 0.92 and 0.89), beverages except for coffee or green tea (ORIQR = 0.97 and 0.96), and bread (ORIQR = 0.96 and 0.94). Men with MetS consumed high total sodium (ORIQR = 1.04), and large amounts of Kimchi (ORIQR = 1.03), fermented paste (ORIQR = 1.04), and noodles (ORIQR = 1.07). Women with MetS consumed more Kimchi than those without MetS (ORIQR = 1.04). The odds ratio for the low calcium and high sodium group compared to the high calcium and low sodium group was 1.26. The MetS group consumed less calcium-rich foods and more sodium-rich foods than those without MetS. Patients with MetS might benefit from precise recommendations of high calcium-rich and low sodium-rich foods.

Dietary Fructose and Sodium Consumed during Early Mid-Life Are Associated with Hypertensive End-Organ Damage by Late Mid-Life in the CARDIA Cohort.

We aimed to investigate how dietary fructose and sodium impact blood pressure and risk of hypertensive target organ damage 10 years later. Data from n = 3116 individuals were obtained from the Coronary Artery Risk Development in Young Adults (CARDIA) study. Four groups were identified based on the four possible combinations of the lower and upper 50th percentile for sodium (in mg) and fructose (expressed as percent of total daily calories). Differences among groups were ascertained and logistic regression analyses were used to assess the risk of hypertensive target organ damage (diastolic dysfunction, coronary calcification and albuminuria). Individuals in the low-fructose + low-sodium group were found to have lower SBP compared to those in the low-fructose + high-sodium and high-fructose + high-sodium groups (p < 0.05). The highest risk for hypertensive target organ damage was found for albuminuria only in the high-fructose + high-sodium group (OR = 3.328, p = 0.006) while female sex was protective across all groups against coronary calcification. Our findings highlight that sodium alone may not be the culprit for hypertension and hypertensive target organ damage, but rather when combined with an increased intake of dietary fructose, especially in middle-aged individuals.

Partial Replacement of NaCl with KCl in Cooked Meat Could Reduce the Liver Damage Through Renin-Angiotensin System in Mice.

Dietary salt (sodium chloride, NaCl) is necessary for processed meat products, but intake of a high-sodium diet carries serious health risks. Considerable studies indicate that the partial substitution of NaCl with potassium chloride (KCl) can produce sodium-reduced cooked meat. However, most studies of sodium-reduced cooked meat focus on the production process in vitro, and the effect of cooked meat on health has not been well clarified in vivo. This study finds that compared to the high-sodium group (HS), serum renin, angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and the levels of some indicators of dyslipidemia are decreased in the reduced salt by partial substitution of NaCl with KCl group (RS+K). Furthermore, RS+K increases the antioxidation abilities, inhibits the renin-angiotensin system (RAS) through ACE/Ang II/Ang II type 1 receptor axis pathway, reduces synthesis of triglyceride and cholesterol and protein expressions of inflammatory factors interleukin-17A and nuclear factor-kappa B in the liver. Partial substitution of NaCl with KCl in cooked meat can be a feasible approach for improving the health benefits and developing novel functional meat products for nutritional health interventions.

Effect of Low and High Sodium Dialysate on Functional Capacity and Health Related Quality of Life in Hemodialysis Patients

Abstract Background Patients on dialysis have low health related quality of life (HRQOL) and an annual mortality rate many-fold greater than the general population. There is uncertainty about whether low sodium in dialysis fluid improves overall health and wellbeing for people on haemodialysis, since there are mixtures of probably good and bad effects. Aim To assess the effect of low sodium and high sodium dialysate on functional capacity and HRQOL in hemodialysis patients. Patients and Methods comparative case-control study conducted on 60 ESRD patients on maintenance hemodialysis receiving their treatment at the Nephrology hemodialysis unit in Luxor International Hospital from June 2021 till November 2021. The study population was divided into 2 groups: Group 1: included 30 patients on low sodium dialysate (130 mmol/l). Group 2: included 30 patients on high sodium dialysate (138 mmol/l). Results Our data revealed a significant increase in the percentage of hypertensive patients recruited to be among the low sodium dialysate group as compared with high sodium group (P value &amp;lt;0.001). At the end of the study, there were a significant decrease in DBP, IDWG and UF among low sodium group compared with high sodium group, there were a significant increase in 6MWT and SF-36 in Low sodium group when compared with High sodium group. No statistical significant difference between the studied groups as regard each of the laboratory data, ECG, and ECHO at the end of the study (P value&amp;gt;0 Conclusion Low sodium dialysate is effective in improving the health related quality of life of hypertensive hemodialysis patients, however, it did not reduce left ventricular mass relative to control despite improving fluid status.

Analysis and identification of ancient glass components based on qualitative-quantitative data mining

First of all, the data is visualized by grouping the data in the form and drawing a scatter diagram. By observing the distribution of the data in the scatter plot, the classification indexes of high-potassium glass and lead-barium glass were found. Secondly, the Spearman coefficient is used to test these classification indicators. The results show that the constructed classification system is more accurate, the Spearman coefficient is small, and the fitting effect is excellent. Secondly, through the combination of qualitative and quantitative methods, the cultural relics sub-category classification index was double screened, and the chemical composition of the sub-category classification index was determined by combining the law analyzed from the scatter plot and the index weight solved by the entropy weight method. Then, the high-potassium glass was divided into low-calcium and low-copper group and high-calcium and high-copper group by K-means method. The glass was divided into high copper group, low sodium and high calcium group and high sodium and low calcium group. Finally, all the unknown types of cultural relics in the table are divided into subclasses, and the sensitivity and rationality of the classification system of major classes and subclasses are tested one by one by fitting the known data and calculating the contour coefficient. It is concluded that the classification system has a good fit to the data.

Evidence for local aldosterone synthesis in the large intestine of the mouse.

Aldosterone, the main physiological mineralocorticoid, regulates sodium and potassium balance in the distal convoluted tubule of the kidney. Aldosterone is synthesized from cholesterol in the adrenal cortex in a sequence of enzymatic steps. Recently however, several tissues or cells e.g. brain, heart, blood vessels, kidneys and adipocytes have been shown to possess capability to produce aldosterone locally, and there is some evidence that this occurs also in the intestine. Colon expresses mineralocorticoid receptors and is capable of synthesizing corticosterone, the second last intermediate on the route to aldosterone from cholesterol. Based on such reports and on our preliminary finding, we hypothesized that aldosterone could be synthesized locally in the intestine and therefore we measured the concentration of aldosterone as well as the protein and gene expression of aldosterone synthase (CYP11B2), an enzyme responsible on aldosterone synthesis, from the distal section of the gastrointestinal tract of 10-week-old Balb/c male mice. It is known that sodium deficiency regulates aldosterone synthesis in adrenal glands, therefore we fed the mice with low (0.01%), normal (0.2%) and high-sodium (1.6%) diets for 14 days. Here we report that, aldosterone was detected in colon and cecum samples. Measurable amounts of CYP11B2 protein were detected by Western blot and Elisa analysis from both intestinal tissues. We detected CYP11B2 gene expression from the large intestine along with immunohistochemical findings of CYP11B2 in colonic wall. Sodium depletion increased the aldosterone concentration in plasma compared to control and high-sodium groups as well as in the intestine compared to mice fed with the high-sodium diet. To summarize, this study further supports the presence of aldosterone and the enzyme needed to produce this mineralocorticoid in the murine large intestine.

Prognostic factors influencing outcome in adult liver transplantation using hypernatremic organ donation after brain death

BackgroundHypernatremic donors was regarded as the expanded criteria donors in liver transplantation. The study was to investigate the effects of donor hypernatremia on the outcomes of liver transplantation and identify the prognostic factors possibly contributing to the poor outcomes. MethodsDonor serum sodium levels before procurement were categorized as normal sodium (< 155 mmol/L), moderate high sodium (155–170 mmol/L), and severe high sodium (≥ 170 mmol/L). Furthermore, we subdivided the 142 hypernatremic donors (≥ 155 mmol/L) into two subgroups: subgroup A, the exposure time of liver grafts from hypernatremia to reperfusion was < 36 h; and subgroup B, the exposure time was ≥ 36 h. The outcomes included initial graft function, survival rates of grafts and recipients, graft loss and early events within the first year following liver transplantation. ResultsThere were no significant differences in the 1-year survival rates of grafts and recipients, 1-year graft loss rates and early events among the normal, moderate high and severe high sodium groups. However, the overall survival rates of grafts and recipients in subgroup A were significantly higher than those in subgroup B. Cox model showed that the exposure time (HR = 1.117; 95% CI: 1.053–1.186; P < 0.001), cold ischemia time (HR = 1.015; 95% CI: 1.006–1.024; P = 0.001) and MELD (HR = 1.061; 95% CI: 1.003–1.121; P = 0.037) were the important prognostic factors contributing to the poor outcomes of recipients with hypernatremic donors. ConclusionsThe level of donor sodium immediately before organ procurement does not have negative effects on the early outcomes following adult liver transplantation. For hypernatremia liver donors, minimization of the exposure time from hypernatremia to reperfusion is critical to prevent graft loss.

A7793 The role of TGF-β1/smad3 pathway on phenotype transformation and collagen synthesis of rat cardiac fibroblasts induced by high sodium

Objectives: In order to research the effects of TGF-β1/smad3 signaling pathway on the phenotype transformation and collagen synthesis of rat cardiac fibroblasts (CFs) induced by high sodium in vitro. Methods: The CCK8 assays were used to determine optimal concentration and action time of smad3 inhibitor (SIS3) and TGF-β1 receptor inhibitor (SB431542) on CFs from Wistar rats. CFs were divided into control group (Na+139 mmol/L), high-sodium group (Na+149 mmol/L- Na+176 mmol/L), high-sodium+SIS3 group (Na+161 mmol/L+SIS3 0.5 μM- 5 μM), high-sodium+SB group (Na+161 mmol/L+SB431542 1 μM- 25 μM), mannitol group (osmotic pressure corresponding to the Na+ 161 mmol/L group), and cultured for 48 h. The mRNA and protein levels of α-SMA, fibronectin extra domain-A (Fn ED-A), Collagen I, Collagen III, TGF-β1, smad3 were detected by real time-PCR, Western blot and immunofluorescence. The content of TGF-β1 in culture supernatant was determined by ELISA. The CFs migration was observed through the cell scratch test. Results: High sodium promoted the proliferation and migration of rat CFs under the exclusion of osmotic pressure. The proliferation of CFs was inhibited in a dose-dependent manner by SIS3 and SB431542. The mRNA and protein levels of α-SMA, Fn ED-A, Collagen I, Collagen III, TGF-β1, p-smad3 were increased in high-sodium group and excluded the influence of osmotic pressure. The secretion of TGF-β1 in culture medium was elevated as well. Meanwhile, the protein levels of α-SMA, Fn ED-A, Collagen I, Collagen III were downregulated by SB431542 and SIS3. Conclusion: High salt can cause the proliferation and phenotype transformation of CFs toward to myofibroblasts and promote collagen synthesis via TGF-β1/ smad3 pathway. TGF-β1/ smad3 may be the key intervention targets for preventing high-salt induced myocardial fibrosis.

Abstract P219: Site-1 Protease-Derived Soluble (Pro)Renin Receptor Contributes to Salt-Sensitive Hypertension via Activation of the Intrarenal RAS

Dahl salt-sensitive (SS) hypertensive rats exhibit increased expression of renal (pro)renin receptor (PRR) and aberrant activation of the intrarenal renin-angiotensin system (RAS) with unclear functional implication. Recent evidence demonstrates that soluble PRR (sPRR) serves as a potential regulator of tubular transport via activating Wnt/ β-catenin pathway in the distal nephron and is derived from the cleavage by site-1 protease (S1P). The present study attempted to define the role of sPRR during salt-sensitive hypertension in SS rats. The effect of S1P inhibitor PF-429242 (PF at 20 mg/kg/d via mini-pump) on blood pressure, proteinuria, and urinary renin were tested in SS rats during high salt loading. In a separate group, a recombinant sPRR (sPRR-His at 20 μg/kg/d) was infused via catheterization of jugular vein to SS rats during PF treatment. In High sodium (HS)-loaded SS rats, administration of PF attenuated the hypertension development (MAP on day 10, HS+PF group: 124.5 ± 4.6 mmHg vs. HS group: 144.1 ± 8.2 mmHg) as assessed by radiotelemetry and proteinuria (HS+PF group: 50.9 ± 5.5 μg/24h vs. HS group: 105.3 ± 7.4 μg/24h). PF treatment reduced HS-stimulated urinary sPRR excretion by 65% in SS rats. Supplement of sPRR restored HS-induced hypertension during PF treatment (MAP on day 10, HS+PF+sPRR-His group: 138.7 ± 6.1 vs. HS+PF group: 124.5 ± 4.6 mmHg) and proteinuria (HS+PF+sPRR-His group: 79.0 ± 5.8 μg/24h vs. HS+PF group: 50.9 ± 5.5 μg/24h) in SS rats. Concurrently, PF treatment reduced HS-stimulated urinary renin activity (by 80%), aldosterone excretion (by 36%) and renal medullary prorenin and renin (by 60%), which were all restored by sPRR-His infusion (1.5- to 3-fold). Indices of Wnt/β-catenin pathway including protein levels of renal cytosolic Axin-2 and nuclear β-catenin as assessed by immunoblotting were elevated by HS (3.4-fold, 2.2-fold respectively) in SS but not SR rats, which were all suppressed by S1P inhibition (by 80% and 50% respectively) and restored by sPRR-His infusion. Given β-catenin signaling as a known regulator of intrarenal RAS, our results suggest that S1P-derived sPRR plays a pathogenic role in salt-sensitive hypertension in SS rats via β-catenin/intrarenal RAS pathway.

Sodium Intake Is associated With Endothelial Damage Biomarkers and Metabolic Dysregulation.

Mounting evidence has associated high sodium (HS) intake with hypertension, cardiovascular disease, and stroke. We investigated whether HS intake modulates the parameters of endothelial damage, inflammation, and oxidative stress. We used a cross-sectional study design including 223 Chilean subjects (6.9-65.0 years old). We measured aldosterone, renin activity, cortisol, cortisone, adiponectin, leptin, hsCRP, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), plasminogen activator inhibitor type 1 (PAI-1), metalloproteinase (MMP)-9 and MMP-2 activity, and malondialdehyde. Sodium and creatinine were measured in 24-hour urine samples. The subjects were divided by sodium intake, high sodium (HS): ≥150 mEq/day, n = 118, and adequate sodium (AS): <150 mEq/day, n = 105. We observed a positive correlation between urinary sodium excretion and blood pressure (r = 0.1669, P = 0.0124 for systolic and r = 0.2416, P = 0.0003 for diastolic), glycemia (r = 0.2660, P < 0.0001), and triglycerides (r = 0.1604, P = 0.0175) and a highly significant correlation between sodium excretion and PAI-1 (r = 0.2701, P < 0.0001). An inverse correlation was observed between urinary sodium and HDL-cholesterol (r = -0.2093, P = 0.0018) and adiponectin (r = -0.2679, P < 0.0001). In a linear regression model, urinary sodium excretion remained significantly associated with PAI-1 values even after adjusting for age, gender, and BMI. The HS group had higher blood pressure, glycemia, HOMA-IR, atherogenic index of plasma, and PAI-1 values than the group with AS intake. HS intake is associated with endothelial damage (high PAI-1) and metabolic dysregulation. On the other hand, inflammation and oxidative stress parameters are not modified by sodium intake.

LEFT VENTRICULAR DIASTOLIC FUNCTION IN RELATION TO SODIUM DIETARY INTAKE AND RENAL HANDLING

Objective: Sodium load has been associated with blood pressure (BP) and target organ damage. Sodium sensitivity of BP varies between individuals and may be determined by renal sodium handling. The present study aimed to investigate ambulatory blood pressure and left ventricular diastolic function in relation to interaction between sodium dietary intake and renal handling. Design and method: We recruited 303 (mean age, 46.9 years; 55% women) members from randomly selected families. The 24-hour blood pressure monitoring was assessed. Left ventricular mass index, left atrium (LA) diameter, and the ratio of early (E) and late (A) diastolic peak of transmitral flow velocities (E/A) as well as the ratio of E to tissue doppler early diastolic mitral annular velocity (Em) were assessed by echocardiography (VIVID 7). Serum and urinary sodium concentration was measured using an automatic analyzer while lithium concentration by automatic absorption spectrometry. The median value of urinary sodium excretion (uNa) and median value of fractional urinary lithium excretion (FELi) - marker of sodium reabsorption in proximal tubules and as a consequence sodium sensitivity - were calculated. Results: To evaluate the influence of high sodium diet on parameters of interest we divided participants on two groups: high sodium group (HNa) constituted 86 participants with uNa above the median value (156.6 mmol/day) and FELi below the median value (16.6%), while the low sodium group (LNa) combined 79 persons with uNa below and FELi above the respective median value. 24-hour systolic and diastolic BP, left atrium diameter and E/Em were higher in HNa group in comparison to LNa participants (p < 0.05). After adjusting for relatedness, age, gender, and antihypertensive treatment, significant differences between predefined groups in 24-hour systolic BP (120.2 vs 117.0 (mmHg), p = 0.03) and E/Em (7.3 vs 6.7(%), p = 0.016) ratio persisted. Conclusions: The study may be the basis for an assumption that in participants with a paradoxical high renal sodium retention in case of sodium overload an impairment of cardiac diastolic function develops sooner, suggesting that a reduction of salt intake may improve cardiac diastolic function.

Moderate salt restriction with or without paricalcitol in type 2 diabetes and losartan-resistant macroalbuminuria (PROCEED): a randomised, double-blind, placebo-controlled, crossover trial

Macroalbuminuria predicts renal and cardiovascular events in patients with type 2 diabetes. We aimed to assess the albuminuria-lowering effects of salt restriction, paricalcitol therapy, or both, in this population. In this randomised, double-blind, placebo-controlled, crossover trial, we recruited adult patients with type 2 diabetes from six diabetology outpatient clinics in northern Italy, with 24 h albuminuria of more than 300 mg despite 100 mg per day losartan therapy, blood pressure of less than 140/90 mm Hg, serum creatinine concentration of less than 2 mg/dL, stable renal function on stable renin-angiotensin system inhibitor therapy with a fixed dose of losartan, parathyroid hormone concentration of 20 pg/mL to <110 pg/mL, serum calcium concentration of less than 9·5 mg/dL, and serum phosphate concentration of less than 5 mg/dL, who had been more than 80% compliant with placebo treatment during a 1 month placebo run-in. We allocated patients 1:1 with computer-generated randomisation to an open-label 3 month high-sodium (>200 mEq [4·8 g] per day) or low-sodium (<100 mEq [2·4 g] per day) diet and, within each diet group, to a 1 month double-blind treatment period of oral paricalcitol (2 μg per day) or placebo, followed by 1 month of placebo washout and then a further 1 month double-blind treatment period of paricalcitol or placebo in which patients crossed over to the opposite treatment period. The primary outcome was 24 h albuminuria (median of three consecutive measurements). Analyses were modified intention-to-treat (including all randomly allocated patients who took at least one dose of study drug and had an efficacy measurement after the first treatment period). Patients and investigators were masked to paricalcitol and placebo assignment. Those assessing outcomes were masked to both study drug and diet assignment. This study is registered with ClinicalTrials.gov, number NCT01393808, and the European Union Clinical Trials Register, number 2011-001713-14. Between Dec 13, 2011, and Feb 17, 2015, we randomly allocated 57 (50%) patients to a low-sodium diet (28 [49%] to paricalcitol then placebo and 29 [51%] to placebo then paricalcitol) and 58 (50%) to a high-sodium diet (29 [50%] to paricalcitol then placebo and 29 [50%] to placebo then paricalcitol). In the low-sodium group (30 mEq of daily sodium intake reduction, equivalent to approximately 1·7-1·8 g per day), 24 h albuminuria was reduced by 36·6% (95% CI 28·5-44·9) from 724 mg (441-1233) at baseline to 481 mg (289-837) at month 3 (p<0·0001), but no significant change occurred in the high-sodium group (from 730 mg [416-1227] to 801 mg [441-1365]; 2·9% [-16·8 to 16·4] increase; p=0·50). Changes between diet groups differed by 32·4% (17·2-48·8; p<0·0001) and correlated with changes in natriuresis (r=0·43; p<0·0001). On the high-sodium diet, paricalcitol reduced the salt-induced albuminuria increase by 17·8% (3·9-32·3) over the month of treatment compared with placebo (p=0·02), whereas on the low-sodium diet, paricalcitol did not have a significant effect versus placebo (increase of 4·1% [-9·3 to 21·6]; p=0·59). During placebo treatment, albuminuria decreased with the low-sodium diet (p=0·0002) and did not significantly change with the high-sodium diet, but changes were significantly different between diet groups (p=0·0004). Treatment was well tolerated and no patients withdrew from the study because of treatment-related effects. 67 adverse events occurred in 52 (45%) patients during paricalcitol treatment and 44 events occurred in 36 (31%) patients during placebo treatment. During paricalcitol therapy, 14 cases of hypercalciuria, six cases of hypercalcaemia, and five cases of hyperphosphataemia were reported in one patient each, all of which were possibly treatment related. One case of hypercalciuria was reported in one patient during the placebo treatment period. One stroke and one coronary event occurred during paricalcitol therapy. No patients died during the study. In patients with macroalbuminuria and type 2 diabetes, moderate salt restriction enhances the antialbuminuric effect of losartan, an effect that could be nephroprotective and cardioprotective in the long term. The finding that paricalcitol prevents a sodium-induced increase in albuminuria provides support for trials to test the long-term risk-benefit profile of paricalcitol add-on therapy in patients with type 2 diabetes and macroalbuminuria refractory to dietary salt restriction, including patients refractory to even moderate salt restriction. AbbVie.

Dietary sodium, dietary potassium, and systolic blood pressure in US adolescents.

Both high sodium and low potassium diets are associated with hypertension, but whether these risk factors are distinct or overlapping has not been thoroughly investigated. The authors evaluated the relationship between dietary sodium, potassium, and high systolic blood pressure among 4716 adolescents aged 12 to 14 years who participated in the National Health and Nutrition Examination Survey from 1999 to 2012. There was no association with blood pressure across most values of sodium or potassium intake. However, participants who reported sodium intake ≥7500mg/d, potassium <700mg/d, or sodium-potassium ratio ≥2.5 had increased odds for high systolic blood pressure (≥95th percentile for age, sex, and height). Although the high sodium and low potassium groups did not overlap, 49.2% of these adolescents also had a sodium-potassium ratio ≥2.5. In young adolescents, both excessive sodium and limited potassium are associated with high systolic blood pressure, but the balance between sodium and potassium intake may be more useful in explaining blood pressure in this population.

Ototoxicity associated with topical administration of diclofenac sodium as an otic drop: An experimental animal study

ObjectivesThe aim of the study is to evaluate the ototoxicity of topical diclofenac sodium in comparison to positive and negative controls prior to the investigation of analgesic and anti-inflammatory efficacy of the agent in otic administration. MethodsTwenty four ears of 12 guinea pigs were included in the study. Wide myringotomy was performed on all tympanic membranes under general anesthesia and auditory brainstem responses (ABR) were evaluated. The subjects were separated into four groups, two groups received diclofenac sodium at low and high doses, positive controls received gentamicin and negative controls received isotonic sodium chloride topically for 14 days and ABRs were reevaluated. ResultsNo significant difference were observed between the pre and post-treatment click response, 1 kHz and 8 kHz response threshold levels after isotonic sodium chloride administration. All threshold levels were elevated in the positive control group. In the low and high dose diclofenac sodium groups, click response, 1 kHz and 8 kHz response threshold levels were significantly higher compared to the baseline values. Pre and post-treatment mean threshold level changes were not significantly different between the low and high dose diclofenac sodium groups. Pre and post-treatment mean threshold level changes in the gentamicin group were not significantly different from low or high dose diclofenac sodium groups. ConclusionDiclofenac sodium, considered as an analgesic and anti-inflammatory otic preparation, is shown to be as ototoxic as gentamicin in chronic use which may lead to loss of hearing especially when used topically in chronic otitis cases with tympanic membrane damage.

Abstract P106: Effects of Aldosterone Excess and Sodium on Dipping Patterns in Resistant Hypertensive Patients

Background: High dietary sodium intake and aldosterone excess have been independently linked to increased cardiovascular morbidity and mortality. In addition, a large body of literature indicates that aldosterone excess contributes importantly to antihypertensive treatment resistance and is associated with higher 24- hour ambulatory blood pressure (BP) levels. Objective: This study was designed to determine if high dietary sodium intake, and hyperaldosteronism combine to mediate the development of abnormal diurnal BP patterns including nocturnal hypertension and dipping BP patterns. Methods: A single-center cohort of 326 African American (AA) and Caucasian resistant hypertensive patients were prospectively evaluated by assessing 24-hr urinary aldosterone (UAldo), plasma renin activity (PRA), sodium (UNa + ) levels, and 24-hr ambulatory blood pressure monitoring (ABPM). Daytime, night-time, and 24-hr BP and dipping patterns were determined. High sodium excretion was defined as UNa + = 200 mEq/24hr and hyperaldosteronism was defined as UAldo = 12 μg/24hr and PRA ≤ 1 ng/ml/hr. Results: There was no difference in ABPM and dipping patterns when comparing the normal versus high sodium group. However, patients without high sodium excretion had better nocturnal (p=0.024) and 24- hour BP control (p=0.036). Furthermore, there was no difference in ABPM patterns when comparing patients with high versus normal sodium excretion with hyper versus non- hyperaldosteronism. Interestingly, in the group with hyperaldosteronism, patients with normal sodium excretion had improved dipping patterns, but only in the dipper group (p=0.016). Conclusions: High dietary sodium intake contributes to increased nocturnal hypertension and poor 24-h BP control, but there does not seem to be a significant relationship between hyperaldosteronism and high dietary sodium intake. This data suggests that improvements in dietary sodium intake will lead to better control of nighttime BP and 24-h BP control and therefore reduces the risk of cardiovascular disease. Further studies are underway comparing these relationships in males versus females, and AAs versus Caucasians.

Relationship of serum sodium level with cerebral edema and prognosis in patients with spontaneous intracerebral hemorrhage

Objective To investigate the association of serum sodium level with cerebral edema and prognosis in patients with spontaneous intracerebral hemorrhage. Methods We prospectively studied 90 patients with spontaneous intracerebral hemorrhage within 24 hours from onset of symptoms. According to the target value of serum sodium level, the patients were divided into 3 groups, relatively low-sodium group (135-140 mmol/L), relatively high-sodium group (140-145 mmol/L), absolute high-sodium group ( 145-155 mmol/L)(n=30 for each). National institutes of health stroke scale (NIHSS), Glasgow coma score (GCS), and blood tests were measured within 24 hours from onset. Hematoma volumes, edema volumes, liver and kidney function were measured within 24 hours, 3 days, 7 days after onset. Modified rankin scale (MRS) were measured at 90 days to assess the recovery of neurological function. Modified rankin scale score ≤ 2 was considered as good outcome. Results The edema volume was smaller in absolute high-sodium group than in relatively low-sodium group and relatively high-sodium group 〔(25.37±26.54) ml vs. (55.21±58.21) ml, (59.48±55.84) ml, F=1.492, P=0.023〕. The percentage of patients with MRS score ≤2 was 70% in absolute high-sodium group, which had a better prognosis as compared with relatively low-sodium and relatively high-sodium group (both P<0.05). The hematoma volume had no significant difference among the three groups. Conclusions The appropriate increase in serum sodium level is safe, which could reduce cerebral edema and get a better prognosis. Key words: Cerebral hemorrhage; Edema; Sodium

High sodium intake is associated with short leukocyte telomere length in overweight and obese adolescents.

Background/ObjectivesTelomere shortening plays an important role in cellular aging. However, the impact of high sodium intake, an important risk factor of age-related diseases, on telomere shortening remains unknown. Therefore, we examined the relationship between high dietary sodium intake and leukocyte telomere length, particularly in the context of obesity since obesity increases salt sensitivity.Subjects/MethodsLeukocyte telomere length (LTL) was determined by a quantitative polymerase chain reaction method in 766 adolescents aged 14–18 years (50% female, 49% African Americans). Dietary sodium intake was assessed by seven independent 24-h dietary recalls. We divided the sample into low sodium (mean 2388 ± 522 mg/day) or high sodium groups (mean 4142 ± 882 mg/day) based on the median value (3280.9 mg/day).ResultsIn the entire cohort, there was no significant association between sodium intake and LTL (r = −0.05, p = 0.24). However, there was a significant interaction between sodium intake and obesity status (p = 0.049). Further multiple linear regression analyses revealed that higher dietary sodium intake was associated with shorter LTL in the overweight/obese group (BMI ≥ 85th percentile, β = −0.37, p = 0.04), but not in the normal weight group (β = 0.01, p= 0.93) after adjusting for multiple confounding factors. In the overweight/obese group, LTL was significantly shorter in the high sodium intake subjects vs. low sodium intake subjects (1.24 ± 0.22 vs. 1.32 ± 0.20, p = 0.02), but not the normal weight group (1.29 ± 0.24 vs. 1.30 ± 0.24, p = 0.69).ConclusionsHigher dietary sodium intake is associated with shorter telomere length in overweight and obese adolescents.

Oxidative Stress and Neuronal NOS Activity: Putative Determinants of Rapid Blood Pressure Increase After Renal Denervation in Anesthetized Rats

Long-term effects of renal denervation (DNX) commonly include a decrease in blood pressure (BP), observed in both normotensive animals and various models of hypertension. On the other hand, short term BP responses vary. We examined how post-DNX increase in BP observed in this study depends on baseline metabolic and functional status of animals, with a special interest for the role of oxidative stress. Anesthetized Wistar rats on standard (STD), low-sodium (LS) or high-sodium (HS) diet were used, untreated or pre-treated with tempol, a superoxide scavenger, or N(omega)-propyl-L-arginine (L-NPA), an inhibitor of neuronal NOS (nNOS). Early BP and renal hemodynamic responses were examined to right- and then left-side DNX performed using an own relatively non-invasive technique. Left kidney cortical, outer- and inner-medullary blood flows (CBF, OMBF, IMBF) were continuously recorded as laser-Doppler fluxes. Sequential denervations significantly increased BP to final 19 %, 12 %, and 6 % above control level in HS, LS, and STD groups, respectively. CBF, a measure of total renal perfusion, increased in LS and STD but not in HS rats. Tempol pretreatment prevented the post-denervation BP increase on each diet. Selective inhibition of nNOS prevented BP increase in STD and HS groups, a modest increase persisted in LS rats. We propose that enhanced afferent impulsation from intrarenal chemoreceptors related to oxidative stress in the kidney was the background for acute BP increase after DNX. The response was triggered by a release of brain sympatho-excitatory centers from inhibition by renal afferents, this was followed by widespread sympathetic cardiovascular stimulation.

High-sodium intake aggravates myocardial injuries induced by aldosterone via oxidative stress in Sprague-Dawley rats

To evaluate the effects of aldosterone with or without high sodium intake on blood pressure, myocardial structure and left ventricular function in rats, and to investigate the mechanisms underlying the effects. Eight-week-old male Sprague-Dawley rats were randomly divided into 3 groups: (1) control (CON) group fed a normal sodium diet, (2) aldosterone (ALD) group receiving aldosterone infusion and a normal sodium diet, and (3) high sodium plus aldosterone (HS-ALD) group receiving 1% NaCl diet in conjunction with aldosterone infusion. Aldosterone was administered through continuously subcutaneous infusion with osmotic minipump at the rate of 0.75 μg/h for 8 weeks. The myocardium structure was observed using transthoracic echocardiography and transmission electron microscopy. The collagen deposition in left ventricle was evaluated with Masson's trichrome staining. The expression of IL-18, p22phox, and p47phox proteins was examined using Western blot analysis. The systolic blood pressure in the ALD and HS-ALD groups was significantly higher than that in the CON group after 2-week treatment. But the blood pressure showed no significant difference between the HS-ALD and ALD groups. The left ventricular hypertrophy, myocardial collagen deposition and oxidative stress were predominantly found in the HS-ALD and ALD group. Furthermore, the breakdown of myocardial structure and oxidative stress were more apparent in the HS-ALD group as compared with those in the ALD group. Long-term infusion of aldosterone results in hypertension and profibrotic cardiovascular responses in rats fed a normal sodium diet, which were mediated by oxidative stress. High-sodium intake could aggravate myocardial injuries induced by aldosterone.