Excess Dietary Salt Intake Research Articles

Enhancing the perception of saltiness and reducing NaCl levels in snacks through sensory interaction: Immobilizing NaCl nanocrystals in Litsea oleoresin-sunflower seed oleogels

Excessive dietary salt intake leads to health issues, while reducing NaCl content compromises flavor. Therefore, identifying methods to decrease salt levels without sacrificing flavor is crucial. This study investigated the sensory interaction between the saltiness of NaCl and the pungency of Litsea oleoresin. Glyceryl monostearate (6.6%) and soy lecithin (4.4%) were used as gelling agents to create oleogels, which were then employed to immobilize NaCl nanocrystals, optimizing sensory interactions. NaCl nanocrystals (427.73 ± 61.98 nm) were encapsulated in a Litsea oleoresin-sunflower seed oleogel system with uniform distribution. Sensory evaluation indicated that the NaCl nanocrystal/Litsea oleoresin@oleogel system, with moderate pungency, significantly enhanced perceived saltiness intensity (29.00 ± 1.14, compared to the control, 18.48 ± 1.12) (P < 0.05). When applied to potato chips, this system noticeably increased saltiness perception. This research provides a promising approach for developing low-sodium yet flavorful foods.

Excess Salt Intake Activates IL-21-Dominant Autoimmune Diabetogenesis via a Salt-Regulated Ste20-Related Proline/Alanine-Rich Kinase in CD4 T Cells.

The fundamental mechanisms whereby a diet affects susceptibility to or modifies autoimmune diseases are poorly understood. Despite excess dietary salt intake acts as a risk factor for autoimmune diseases, little information exists on the impact of salt intake on type 1 diabetes. To elucidate the potential effect of high-salt intake on autoimmune diabetes, non-obese diabetic (NOD) mice were fed with a high-salt diet (HSD) or a normal-salt diet from 6 to 12 weeks of age and monitored for diabetes development. Our results revealed that HSD accelerated diabetes progression with more severe insulitis in NOD mice in a CD4+ T cell-autonomous manner when compared to NSD group. Moreover, expression of IL-21 and SPAK in splenic CD4+ T cells from HSD-fed mice was significantly upregulated. Accordingly, we generated T cell-specific SPAK knockout (CKO) NOD mice and demonstrated that SPAK deficiency in T cells significantly attenuated diabetes development in NOD mice by downregulating IL-21 expression in CD4+ T cells. Furthermore, HSD-triggered diabetes acceleration was abolished in HSD-fed SPAK CKO mice when compared to HSD-fed NOD mice, suggesting an essential role of SPAK in salt-exacerbated T cell pathogenicity. Finally, pharmacological inhibition of SPAK activity using a specific SPAK inhibitor (closantel) in NOD mice ameliorated diabetogenesis, further illuminating the potential of a SPAK-targeting immunotherapeutic approach for autoimmune diabetes. Here, we illustrate that a substantial association between salt sensitivity and the functional impact of SPAK on T cell pathogenicity serves as a central player linking high-salt intake influences to immune-pathophysiology of diabetogenesis in NOD mice.

Physiological Mechanisms of Dietary Salt Sensing in the Brain, Kidney, and Gastrointestinal Tract.

Excess dietary salt (NaCl) intake is strongly correlated with cardiovascular disease and is a major contributing factor to the pathogenesis of hypertension. NaCl-sensitive hypertension is a multisystem disorder that involves renal dysfunction, vascular abnormalities, and neurogenically-mediated increases in peripheral resistance. Despite a major research focus on organ systems and these effector mechanisms causing NaCl-induced increases in arterial blood pressure, relatively less research has been directed at elucidating how NaCl is sensed by various tissues to elicit these downstream effects. The purpose of this review is to discuss how the brain, kidney, and gastrointestinal tract sense NaCl including key cell types, the role of NaCl versus osmolality, and the underlying molecular and electrochemical mechanisms.

Physicochemical properties and consumer acceptance of sodium-reduced condiment from fermented horse gram (Macrotyloma uniflorum)

Excessive dietary salt intake is associated with the development of hypertension, causing millions of deaths around the world annually. Meanwhile, food insecurity caused by rapid growth of global population has drawn researchers’ interest in exploiting underutilized legumes as food resources. Hence, the aim of this study was to develop a novel sodium-reduced condiment from a neglected legume, horse gram (Macrotyloma uniflorum). Different formulations of fermented horse gram condiment (FHGC) were developed by gradual reduction of NaCl content. Nutritional composition and quality parameters of FHGC were assessed in present study. The results showed that amino acid nitrogen content and free amino acid content were both inversely related to NaCl concentration of FHGC. Sensory test conducted revealed that FHGC-12 had the highest consumer acceptability. However, penalty analysis suggested that saltiness was a less significant factor in affecting consumer liking of FHGC. Optimizing the balance of umami, sweet and bitter taste amino acids, in conjunction with NaCl is crucial in affecting acceptability of FHGC, rather than having the highest quantity ratio of amino acids. Therefore, it is imperative to maintain a well-balanced ratio of these key taste components to enhance consumer acceptance of FHGC.

A candidate locus in the renalase gene and susceptibility to blood pressure responses to the dietary salt.

High dietary salt confers a risk of elevating blood pressure (BP) and the development of hypertension. BP to salt intake may be determined in part by individual genetic predisposition. Identifying these genetic underpinnings will enhance our understanding of the biological mechanisms of BP regulation. This study aims to assess the genetic association with salt sensitivity of BP (SSBP) within two well-phenotyped multinational cohorts. A total of 720 white participants from the HyperPATH consortium program were selected and genotyped using a multiethnic genotyping array. Individuals consumed two study diets containing high (>200 mEq/day) and low (<10 mEq/day) sodium content, after which SSBP, aldosterone, and plasma renin activity (PRA) were assessed in a controlled inpatient research setting. A top signal (rs10887801; beta = 4.57, P = 5.03E - 07) at the renalase gene ( RNLS ) region was significantly associated with SSBP. We also identified seven single nucleotide variants with linkage disequilibrium to the top signal at this region that comprised a significant haplotype (TCTTAGTT, P = 0.00081). Homozygous carriers of the T-risk allele of the key single nucleotide variant had higher SSBP ( P ≤ 0.00001) and lower PRA ( P = 0.0076) compared with the nonrisk allele. We identified significant associations between genetic variants of the RNLS gene and BP responses to dietary salt intervention and PRA that suggest susceptibility to volume-driven hypertension. These findings may contribute to a better understanding of the genetic mechanisms underlying BP regulation, support the role of RNLS in the pathogenesis of SSBP, and identify individuals who may be at risk from excess dietary salt intake.

Protocol for the implementation and evaluation of a community-based behavior change intervention to reduce dietary salt intake in India.

Excess dietary salt intake is well established as a leading cause of high blood pressure and associated cardiovascular disease, yet current salt intake in India is nearly 11g per day, more than twice World Health Organization maximum recommended intake of 5g per day. Although dietary survey data from India indicate that the main sources of dietary salt are salt added during cooking at home, and few salt reduction efforts have focused on interventions at the household level. As a result, there is little evidence of the effectiveness of behavior change programs to reduce salt intake at the household level. The study aims to develop and implement a community based behavioral change intervention to reduce salt intake delivered by front line community-based health volunteers; and evaluate the preliminary effectiveness, acceptability, and feasibility of delivering a salt reduction behavior change program and potential to support future scale-up. The study is a pre-post intervention design, and outcomes will be evaluated from a random sample of 1500 participants from 28 villages in two primary health centers in Siddipet, Telangana. Primary outcome is change in salt-related KAB (knowledge, attitude, and behavior) score, and secondary outcomes will be changes in salt intake measured by 24h urinary sodium excretion and change in scores using the subscales of the COM-B ("capability", "opportunity", "motivation" and "behavior") tool. Findings will be used to inform future public health policies to support implementation of scalable community-based interventions to reduce salt intake and control hypertension, the leading-cause of death in India.

Excessive Dietary Salt Intake Exacerbates Cognitive Impairment Progression and Increases Dementia Risk in Older Adults.

To investigate excessive dietary salt intake as an independent risk factor of cognitive impairment and dementia in older adults. Prospective, population-based cohort study. Two thousand forty-one community residents aged ≥60years were recruited between April 2007 and August 2009 from the Shandong area of China. Participants were classified into low, mild, moderate, and high salt intake groups according to urinary sodium measurements for 7 consecutive days. Global cognitive function was assessed at baseline and biennially thereafter using the Mini Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Dementia Rating Scale (DRS), and Informant Questionnaire on Cognitive Decline in the Elderly. Demographics and apolipoprotein E (APOE) genotype were also obtained for each participant. Participants were monitored for 11.4 ± 2.0years. During follow-up, MMSE, MoCA, and DRS scores decreased progressively faster with increasing salt intake (Padjustment < 0.05 among all intake groups). In total, 319 participants (13.74 per 1000 person-years) developed cognitive impairment. Compared with the low salt intake group, cognitive impairment risk was increased by 75% in the mild group (Padjustment= 0.027), 180% in the moderate group (Padjustment < 0.001), and 330% in the high group (Padjustment < 0.001) after adjustment for age, education, mean, and variability in visit-to-visit systolic and diastolic blood pressure, and APOE genotype. The hazard ratio for cognitive impairment increased by 1.59 (95% CI 1.40-1.79) with each 1-SD increment in salt intake after confounder adjustment (Padjustment < 0.001). Excessive dietary salt impairs cognitive function and increases cognitive impairment risk in older adults independently of known risk factors, including hypertension and APOE genotype.

PS-BPP06-4: AGE-DEPENDENT INCREASE IN DIETARY SALT INTAKE IN THE JAPANESE ADULTS

Objective: More than half of all cardiovascular disease deaths have been attributed to high blood pressure. Although numerous factors are involved in the development of hypertension, excess dietary salt intake is quite important because it is a modifiable factor. Obviously, tracking alterations in salt intake with age is important for developing population-based strategies to lower salt intake. However, how salt intake changes with age at the individual level has not been intensively studied in the general population. Thus, the present study was designed to investigate changes in salt intake with age in individuals in the general population. Design and Methods: In this observational follow-up study, apparently healthy men and women age &gt; 30 years who participated in a baseline medical checkup (2008–2009) at our center and had a medical checkup 10 years later (n = 2598) were enrolled. Salt intake was estimated by spot urine analysis. Yearly changes in salt intake were also assessed in participants with complete annual data over the course of 10 years from baseline (n = 1543). Results: The follow-up study demonstrated increased salt intake (8.8 ± 2.0 to 9.3 ± 2.1 g/day, P &lt; 0.001) with increasing age (54.0 ± 9.7 to 64.0 ± 9.8 years). Salt intake increased year over year in participants who had a health checkup annually for the 10-year follow-up period (n = 1543; analysis of variance, P &lt; 0.001). The increase in salt intake with age correlated with an increase in blood pressure. Then, regional levels of salt intake in the baseline period (between July 2008 and June 2009) and the period 10 years later (between July 2018 and June 2019) were compared using cross-sectional analyses. The propensity-matched model revealed similar regional levels of salt intake in the baseline period (8.9 ± 2.0 g/day, 55.8 ± 11.1 years, n = 5018) and at 10 years (8.8 ± 2.0 g/day, P = 0.21; 55.9 ± 13.0 years, P = 0.65, n = 5105). Conclusions: Dietary salt intake gradually increased with age in men and women in the general population during the 10-year follow-up period. This should be considered in devising for population-based strategies to lower dietary salt intake.

Fumarate hydratase as a potential target to ameliorate salt sensitive hypertension

Salt sensitive hypertension is a major risk factor for stroke, heart failure, and end-stage renal disease. The development of salt sensitive hypertension is involved in genetic and environmental factors. Excessive dietary salt intake is known as a main risk factor and one of the most important environmental determinants, exacerbates the salt sensitive hypertension by a renal redox metabolism.

Hypertension, Anxiety and Obstructive Sleep Apnea in Cardiovascular Disease and COVID-19: Mediation by Dietary Salt.

This perspective paper used a grounded theory method to synthesize evidence proposing that sodium toxicity from excessive dietary salt intake is a potential common pathophysiological mechanism that mediates the association of hypertension, obstructive sleep apnea, and anxiety with cardiovascular disease and COVID-19. Increased anxiety in these conditions may be linked to a high-salt diet through stimulation of the sympathetic nervous system, which increases blood pressure while releasing catecholamines, causing a “fight or flight” response. A rostral shift of fluid overload from the lower to the upper body occurs in obstructive sleep apnea associated with COVID-19 and cardiovascular disease, and may be related to sodium and fluid retention triggered by hypertonic dehydration. Chronic activation of the renin-angiotensin-aldosterone system responds to salt-induced dehydration by increasing reabsorption of sodium and fluid, potentially exacerbating fluid overload. Anxiety may also be related to angiotensin II that stimulates the sympathetic nervous system to release catecholamines. More research is needed to investigate these proposed interrelated mechanisms mediated by dietary salt. Furthermore, dietary interventions should use a whole-food plant-based diet that eliminates foods processed with salt to test the effect of very low sodium intake levels on hypertension, anxiety, and obstructive sleep apnea in cardiovascular disease and COVID-19.

Abstract P050: Loss-of-function Cyp4a11 Variants Are Associated With Apparent Treatment Resistant Hypertension Identified In Electronic Medical Records; In The VA Million Veteran’s Program And Vanderbilt’s BioVU

Excessive dietary salt intake is common in patients with and salt-sensitivity contributes to the pathophysiology of resistant hypertension. Dietary salt intake regulates the excretion of 20-HETE and patients with salt-sensitive hypertension have a disrupted relationship between 20-HETE and sodium excretion. We hypothesized that rs1126742, a loss-of-function variant in the gene CYP4A11 encoding the enzyme responsible for the formation of 20-HETE, as well as a more common variant rs3890011, in partial linkage disequilibrium with rs1126742, would be associated with apparent-treatment resistant hypertension (ATRH). To test this hypothesis, we used the Department of Veteran Affairs Million Veterans Program dataset derived from electronic medical records. Patients with ATRH (cases, n=16,833), defined as uncontrolled BP of at least 140/90 mmHg despite the concurrent use of three antihypertensive medications including a thiazide diuretic or patients on four or more antihypertensive medications including a thiazide diuretic, and patients with controlled BP (controls, n=53,931) less than 135/90 mmHg on one or two antihypertensive medications were identified from the dataset using electronic algorithms. Within this population we found that there was a significant association between both rs1126742 and rs3890011 and ATRH (β=0.04, p=0.02; β=0.05, p&lt;0.001, respectively). When we stratified the population by race, rs3890011 was significantly associated with ATRH in both whites and blacks (β=0.04, p&lt;0.001 and β=0.06, p=0.02, respectively) while rs1126742 was associated with ATRH in blacks (β=0.07, p=0.01) but not whites. To validate these findings, we sought replication in an independent site, the Vanderbilt University Medical Center’s BioVU, a DNA databank linked with electronic medical records. We identified white patients with ATRH (n=2,998) and controlled hypertension (n=934), defined as patients with BP controlled to less than 140/90 mmHg by a single antihypertensive medication. The previous associations in whites were replicated; rs3890011 (β=0.43, p=0.02) was significantly associated with resistant hypertension while rs1126742 was not. Our findings support an association between these CYP4A11 loss-of-function variants and ATRH.

GONADOECTOMY REDUCED THE DEGREE OF DEVELOPMENT OF RENOVASCULAR HYPERTENSION IN FEMALE RATS CAUSED BY STOP OF HIGH-SALT DIET

Objective: Excessive dietary salt intake is associated with an increased risk for hypertension. However, more research on measurement, storage and kinetics of sodium on blood pressure and sex hormones is required for dietary salt restrictions. The aim was to study the influence of gonadoectomy and stop of the high-salt diet on the development of renovascular hypertension (RVH) in female rats. Design and method: Was used the model of RVH 1 kidney 1 clip (1K1C) on female Wistar rats. All manipulations with animals were carried out according to the Council Directive 86/609/EEC principles. Gonadoectomized and normal rats of 8 weeks old (eight groups) were used. |There were two control groups: one with gonads © and one without (OvE). 4 groups out of remaining 6 groups of rats, had a high salt diet (4%). All rats from 6 groups the Goldblatt’s (1K1C) surgery was subjected. We had two groups with RVH with normal diet (0,25 % NaCl - RVH and OvE-RVH; two groups with high salt diet - RVH-HS and OvE-RVH-HS; and two groups with high salt diet, which was stop in two weeks after the Goldblatt’s (1K1C) surgery: RVH-ChHS and OvE-RVH-ChHS. In all animals the systemic blood pressure (mBP), diastolic (dBP), systolic (sBP) pressure, left ventricular pressure (LVP) and heart rate was directly measured. Left ventricular hypertrophy (LVH) was calculated as (LVweight)/(rat b.w.)*100%. Results: In all RVH groups, with and without gonads, the systemic arterial hypertension was developed. The most level of RVH was in RVH-ChHS rats: mBP - 145,7 ± 9,5 mmHg, dBP - 123,5 ± 10,4 mmHg, LVH - 0,214 ± 0,013 %. Ovariectomy leads to significant (p &lt; 0,05) decrease in the degree of development of RVH. In OvE-RVH-ChHS was mBP 122,2 ± 6,3 mmHg, dBP 94,0 ± 6,0 mmHg and LVH 0,182 ± 0,009 %. Conclusions: Changing the diet from high salt to normal during the development of renovascular hypertension in female rats leads to an increase in the degree of disease. This effect was not observed in gonadoectomized female rats.

The Dropsy of Popes (1555–1978): A Bad Prognostic Sign Foreboding of Death

The purpose of this study is to explore the historical background of edema as a prognostic sign in popes, a special category of medical subjects whose health status was closely monitored and chronicled because of their unique important status in the events of their times. Nine out of 51 popes, who reigned in the years 1555–1978, died edematous at a mean age of 75.5 years of age. The cause of edema was: heart failure for John Paul I, liver disease, obstructive nephropathy associated with anemia for Paul IV, who also suffered from deep vein thrombosis, and malnutrition for Innocent XIII. Chronic kidney disease due to renal stones of gouty origin caused edema in Clement VIII, Clement X, Clement XI, and Benedict XIV. Obstructive nephropathy due to renal stones of non-gouty origin caused edema in Clement XIII, whereas toxic nephropathy due to the use of mercurials caused edema in Clement XIV. Innocent XI, Benedict XIV, and Clement XIV were bled before death because of impending pulmonary edema. It is not surprising that chronic kidney disease was a significant cause of edema in popes with chronic kidney disease which is associated with impaired sodium excretion. The edema was likely aggravated by the excessive dietary salt intake of the period when the importance of sodium chloride restriction was still not discovered and effective diuretic agents were not available.

Metabolomic Kidney Input and Output Analyses in Salt‐Sensitive Hypertension

RationaleSalt‐sensitive hypertension is globally widespread and associated with increased risk of cardiovascular eventsand kidney disease. Although excess dietary salt intake is a major cause of these damaging effects, many of the underlying mechanisms remain poorly defined. Specifically, it is not understood how the critical energy needs of the kidney are met in face of constantly changing environmental nutrients and how this affects metabolic homeostasis in the kidney.MethodsWe hypothesized that a high salt diet in normal salt‐insensitive Sprague Dawley rat would lead to alterations of renal tubular bioenergetics and substrate metabolism. To test this, metabolomic analysis of arterial plasma (input) and renal venous plasma (filtered output) obtained from unanesthetized instrumented rats was performed using tandem mass spectrometry for comparison on a Q‐Exactive Orbitrap mass spectrometer coupled to a dual‐channel Vanquish Ultra‐Performance Liquid Chromatography system. Plasma metabolites were extracted from 20 µL of plasma from SD rats consuming low salt (0.4% NaCl) or high salt (4% NaCl) for 7, 14, or 21 days. These samples were then analyzed with separation over a hydrophobic (C18) and hydrophilic (HILIC) column under both positive and negative polarity to maximize identification of metabolites identified. Varying amounts of quality control plasma sample pools were used to determine injection sample concentration to analyze for each sample and remaining pools were used for normalization of the runs over time.ResultsA total of 4,603 metabolite features were detected, with 1,205 being identified named compounds. After applying further stringency filters to these named metabolites, 350 were significantly different in response to the varying high salt diets (p &lt;0.05; Benjamini‐Hochberg correction) in at least one of the group comparisons performed (versus low salt and artery versus vein). Differential metabolites include numerous lipids, amino acids, and bioenergetic compounds, among others. There appeared to be a shift in these differential compounds between 14 and 21 days of high salt diet, suggesting a potential metabolic shift between initial responses and prolonged high salt responses. Complementary studies are also underway to compare urine metabolite flux, outer medulla, and cortex in conjunction with the plasma analysis to produce a complete computational prediction model.ConclusionTogether, implementation of this methodology will provide key insights and be valuable in further predicting the emergent properties of complex metabolic interactions in the kidney of rats during the development of salt‐induced hypertension.

Inhibition of Microbiota-dependent Trimethylamine N-Oxide Production Ameliorates High Salt Diet-Induced Sympathetic Excitation and Hypertension in Rats by Attenuating Central Neuroinflammation and Oxidative Stress.

Excessive dietary salt intake induces neuroinflammation and oxidative stress in the brain, which lead to sympathetic excitation, contributing to hypertension. However, the underlying mechanisms remain elusive. Accumulating evidence reveals that trimethylamine-N-oxide (TMAO), a gut microbiota-derived metabolite, is implicated in the pathogenesis of multiple cardiovascular diseases. The present study sought to determine whether central TMAO is elevated and associated with neuroinflammation and oxidative stress in the brain after long-term high salt (HS) diet intake and, if so, whether inhibition of TMAO generation ameliorates HS-induced sympathetic excitation and hypertension. Sprague–Dawley rats were fed either a HS diet or a normal salt (NS) diet and simultaneously treated with vehicle (VEH) or 1.0% 3,3-Dimethyl-1-butanol (DMB, an inhibitor of trimethylamine formation) for 8 weeks. HS + VEH rats, compared with NS + VEH rats, had elevated TMAO in plasma and cerebrospinal fluid (CSF), increased blood pressure (BP), and increased sympathetic drive as indicated by the BP response to ganglionic blockade and plasma norepinephrine levels. HS-induced these changes were attenuated by DMB, which significantly reduced TMAO in plasma and CSF. Neuroinflammation as assessed by proinflammatory cytokine expression and NF-κB activity and microglial activity, and oxidative stress as measured by NAD(P)H oxidase subunit expression and NAD(P)H activity and reactive oxygen species (ROS) production in the hypothalamic paraventricular nucleus (PVN) were increased in HS + VEH rats but were decreased by DMB. DMB had no effects on above measured parameters in NS rats. The results suggest that long-term HS diet intake causes elevation in TMAO in the circulation and brain, which is associated with increased neuroinflammation and oxidative stress in the PVN, an important cardiovascular regulatory center. Inhibition of TMAO generation ameliorates HS-induced sympathetic excitation and hypertension by reducing neuroinflammation and oxidative stress in the PVN.

Effects of almonds on ameliorating salt-induced hypertension in dahl salt-sensitive rats.

Excessive dietary salt intake is related to an increased risk of hypertension. Dietary functional foods probably could help to improve salt-induced hypertension. In this study, Dahl salt-sensitive (DSS) rats were used to investigate their metabolic differences from those of salt-resistant SS.13BN rats and determine whether dietary protein-rich almonds could ameliorate salt-induced elevation of blood pressure in DSS rats. After high-salt intake, the systolic blood pressure and mean arterial pressure of the DSS rats increased dramatically. Metabolomics analysis indicated abnormal amino acid metabolism in their kidneys. Their renal nitric oxide (NO) content and nitric oxide synthase activity decreased significantly after high-salt diet. Oxidative stress also occurred in DSS rats. After the DSS rats received almond supplementation, the levels of various amino acids in their kidney increased, and renal arginine and NO contents were upregulated. Their renal hydrogen peroxide and malonaldehyde levels decreased, whereas renal catalase, superoxide dismutase and glutathione peroxidase activities and glutathione levels increased. The renal abnormal amino acid metabolism of DSS rats contributed to the impaired NO production in response to high-salt intake. Together with salt-induced oxidative stress, high-salt diet intake ultimately led to an increase in the blood pressure of DSS rats. Protein-rich almond supplementation might prevent the development of salt-induced hypertension by restoring arginine and NO regeneration and alleviating salt-induced oxidative stress. © 2021 Society of Chemical Industry.

Current Knowledge and Behavior towards Salt Reduction among Hong Kong Citizens: A Cross-Sectional Survey.

Excessive dietary salt intake is prevalent in the Hong Kong community. Over the last decade, the Hong Kong Special Administrative Region Government has been actively promoting community participation to reduce salt intake. The aim of this study was to investigate the current knowledge levels and behaviors relating to dietary salt intake among Hong Kong adults. This cross-sectional survey involved 426 adults in Hong Kong. The findings of this study identified areas of knowledge deficit in the recommended upper limit of daily salt intake for an adult set by World Health Organization (n = 295, 69.2%) indicated a lack of awareness that the overconsumption of salt could cause coronary heart disease (n = 233, 54.7%). Disengagement with salt reduction behavior, such as rarely/never checking the sodium or salt content listed on the food label (n = 252, 59.2%) and rarely/never purchasing food labelled with low salt or no salt content (n = 292, 68.9%), was reported. Excessive salt intake in dietary habits remains an under-recognized non-communicable disease threat by Hong Kong citizens, indicating ineffective responsive risk communication. There is a need to refine existing salt reduction initiatives to aid in making appropriate decisions regarding dietary salt intake among Hong Kong citizens.

Abstract MP22: Dietary Salt Restriction And High Salt Intake Exaggerate Sympathetic Reflexes And Sensitize Central Autonomic Networks: Potential Mechanisms Of The J-shaped Curve

Observational cohort studies suggest that severe salt restriction increases cardiovascular morbidity/mortality, and the relationship between cardiovascular morbidity and dietary salt intake resembles a J-shaped curve. A high salt diet exaggerates sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses to several cardiovascular reflexes in salt-resistant animals. This study assessed whether salt restriction also exaggerates cardiovascular reflex responses and sensitizes central autonomic networks. To test this hypothesis, male Sprague-Dawley rats were fed low (0.01% NaCl), normal (0.1% NaCl), and high (4.0% NaCl) salt diet for 14-21 days. Baseline mean ABP was not different across groups (low: 104±4, normal: 107±4, high: 107±4mmHg). Activation of sciatic afferents (1ms pulse, 500uA, 5s duration, 2-20Hz) produced significantly greater increases in renal SNA (5Hz; low: 196±12, normal: 136±9, high: 177±8%, n=8, P&lt;0.05) and ABP (5Hz; low: 29±3, normal: 16±1, high: 24±2 mmHg, n=8, P&lt;0.05) of rats fed low and high versus normal NaCl diets. Activation of the aortic depressor nerve (2ms pulse, 500uA, 15s duration, 2-20Hz) produced significantly greater decreases in renal SNA (5Hz; low: -55±9, normal: -34±8, high: -63±13%, n=7-8, P&lt;0.05) and ABP (5Hz; low: -31±3, normal: -15±5, high: -32±5 mmHg, n=7-8, P&lt;0.05) of rats fed low and high versus normal NaCl diets. To test whether dietary salt intake sensitized central sympathetic circuits, microinjection of L-glutamate (0.1-1nmol, 30nL) in the rostral ventrolateral medulla produced significantly greater increases in renal SNA (0.1nmol; low: 212±15, normal: 149±8, high: 183±17%, n=7-8, P&lt;0.05) and ABP (0.1Hz; low: 20±2, normal: 12±2, high: 22±2 mmHg, n=7-8, P&lt;0.05) of rats fed low and high versus normal NaCl diets. Finally, rats fed low or high NaCl versus normal NaCl diets displayed exaggerated cardiovascular responses to cage switch or mild restraint and increased 24-h blood pressure variability. The present findings show that severe salt restriction and excess dietary salt intake exaggerate sympathetic and cardiovascular responses, and may be explained by a parallel change in the sensitivity of central autonomic networks to resemble a J-shaped curve.

Elabela Protects Spontaneously Hypertensive Rats From Hypertension and Cardiorenal Dysfunctions Exacerbated by Dietary High-Salt Intake.

Objectives: Arterial hypertension, when exacerbated by excessive dietary salt intake, worsens the morbidity and mortality rates associated with cardiovascular and renal diseases. Stimulation of the apelinergic system appears to protect against several circulatory system diseases, but it remains unknown if such beneficial effects are conserved in severe hypertension. Therefore, we aimed at determining whether continuous infusion of apelinergic ligands (i.e., Apelin-13 and Elabela) exerted cardiorenal protective effects in spontaneously hypertensive (SHR) rats receiving high-salt diet.Methods: A combination of echocardiography, binding assay, histology, and biochemical approaches were used to investigate the cardiovascular and renal effects of Apelin-13 or Elabela infusion over 6 weeks in SHR fed with normal-salt or high-salt chow.Results: High-salt intake upregulated the cardiac and renal expression of APJ receptor in SHR. Importantly, Elabela was more effective than Apelin-13 in reducing high blood pressure, cardiovascular and renal dysfunctions, fibrosis and hypertrophy in high-salt fed SHR. Unlike Apelin-13, the beneficial effects of Elabela were associated with a counter-regulatory role of the ACE/ACE2/neprilysin axis of the renin-angiotensin-aldosterone system (RAAS) in heart and kidneys of salt-loaded SHR. Interestingly, Elabela also displayed higher affinity for APJ in the presence of high salt concentration and better resistance to RAAS enzymes known to cleave Apelin-13.Conclusion: These findings highlight the protective action of the apelinergic system against salt-induced severe hypertension and cardiorenal failure. As compared with Apelin-13, Elabela displays superior pharmacodynamic and pharmacokinetic properties that warrant further investigation of its therapeutic use in cardiovascular and kidney diseases.

GENETICALLY, DIETARY SODIUM INTAKE IS CAUSALLY ASSOCIATED WITH SALT-SENSITIVE HYPERTENSION RISK IN A COMMUNITY-BASED COHORT STUDY: A MENDELIAN RANDOMIZATION APPROACH

Objective: Excessive dietary salt intake is associated with an increased risk of hypertension. Salt sensitivity, i.e., an elevation in blood pressure in response to high dietary salt intake, has been associated with a high risk of cardiovascular disease and mortality. We investigated whether a causal association exists between dietary sodium intake and hypertension risk using Mendelian randomization (MR). Design and method: We performed an MR study using data from a large genome-wide association study comprising 15,034 Korean adults in a community-based cohort study. A total of 1,282 candidate single nucleotide polymorphisms associated with dietary sodium intake, such as rs2960306, rs4343, and rs1937671, were selected as instrumental variables. The inverse variance weighted method was used to assess the evidence for causality. Results: Higher dietary sodium intake was associated with salt-sensitive hypertension risk. The variants of SLC8E1 rs2241543 and ADD1 rs16843589 were strongly associated with increased blood pressure. In the logistic regression model, after adjusting for age, gender, smoking, drinking, exercise, and body mass index, the GRK4 rs2960306TT genotype was inversely associated with hypertension risk (OR = 0.356, 95% CI = 0.236–0.476). However, the 2350GG genotype (ACE rs4343) exhibited a 2.11-fold increased hypertension risk (OR = 2.114, 95% CI = 2.004–2.224) relative to carriers of the 2350AA genotype, after adjusting for confounders. MR analysis revealed that the odds ratio for hypertension per 1 mg/day increment of dietary sodium intake was 2.24 in participants with the PRKG1 rs12414562 AA genotype. Conclusions: Our findings suggest that dietary sodium intake may be causally associated with hypertension risk.