Effect Of Salt Intake Research Articles

The impact of salt consumption on cardiometabolic and cognitive health in aged female rats

Health concerns about excess dietary salt have traditionally focused on its relationship with hypertension and the increased risk of cognitive impairment. However, research has often overlooked the unique health concerns and physiological differences between men and women, leading to gaps in knowledge, particularly regarding disease prevention and treatment strategies for women. The present study examined aged female rats over 12 weeks, using control, low, and high salt diets to mimic the post-menopausal phase in human females when cardiovascular risks typically increase. Cardiometabolic parameters and cognition were monitored. The findings revealed the impact of varying salt diets on blood lipids, blood pressure (BP) and heart rate (HR) levels and variability, anxiety, and cognition. Specifically, intake of a low-salt diet led to a significant reduction in BP levels but an increase in BP variability starting from the eighth week of the diet onset. Moreover, HR levels and variability were notably higher with the low-salt diet. Aged female rats exhibited increased anxiety on the low-salt diet at the fourth week, but the anxiety began to improve starting from the eighth week. Additionally, a trend suggested that the low salt intake worsened short-term memory while improving long-term memory. Furthermore, plasma lipids decreased significantly in aged female rats on a high-salt diet compared to those on a low-salt diet. The study provides valuable insights into the effects of salt intake on cardiometabolic parameters and cognitive function in aged female rats, highlighting the importance of considering sex-specific dietary guidelines for cardiometabolic and cognitive health.

Effects of Salt Intake on 24-Hour Blood Pressure and Gut Microbiome in Women at Midlife: Protocol of a Randomized Controlled-Feeding Study

Effects of Salt Intake on 24-Hour Blood Pressure and Gut Microbiome in Women at Midlife: Protocol of a Randomized Controlled-Feeding Study

Salt Sensitivity: Causes, Consequences, and Recent Advances.

Salt (sodium chloride) is an essential nutrient required to maintain physiological functions. However, for most people, daily salt intake far exceeds their physiological need and is habitually greater than recommended upper thresholds. Excess salt intake leads to elevation in blood pressure which drives cardiovascular morbidity and mortality. Indeed, excessive salt intake is estimated to be responsible for ≈5 million deaths per year globally. For approximately one-third of otherwise healthy individuals (and >50% of those with hypertension), the effect of salt intake on blood pressure elevation is exaggerated; such people are categorized as salt sensitive and salt sensitivity of blood pressure is considered an independent risk factor for cardiovascular disease and death. The prevalence of salt sensitivity is higher in women than in men and, in both, increases with age. This narrative review considers the foundational concepts of salt sensitivity and the underlying effector systems that cause salt sensitivity. We also consider recent updates in preclinical and clinical research that are revealing new modifying factors that determine the blood pressure response to high salt intake.

PS-BPP06-7: ASSOCIATION BETWEEN SALT INTAKE AND BLOOD PRESSURE IN COMMUNITY-DWELLING OLDER PEOPLE: THE SONIC STUDY

Objective: It is well known that excessive salt intake is associated with hypertension (HT) and salt intake reduction lowers blood pressure. However, the knowledge of salt intake and blood pressure in the older people is not sufficient. This study aimed to clarify the relationship between salt intake and blood pressure among community-dwelling Japanese older people. Design and method: This study was cross-sectional design based on a prospective cohort study called the SONIC (Septuagenarians, Octogenarians and Nonagenarians Investigation with Centenarians) study. We used data collected from 2010 to 2012. The dependent variable was the blood pressure at the venue and the independent variable was salt intake. Salt intake was calculated using the brief-type self-administered diet history questionnaire (BDHQ). After adjustment for energy using the residual method, Salt intake was classified into quartiles. Blood pressure values for each quartile were compared by Jonckheere-Terpstra test. Results: The number of participants was 2,163 (female: 53.3%). Persons who may have over- or under-reporting nutrition and had no blood pressure data was excluded. Participants of 70 ± 1 years old were 947 (HT: 50.2%), 80 ± 1 years old were 951 (HT: 63.9%), 90 ± 1 years old were 265 (HT: 50.6%). There was no clear difference of systolic blood pressure among the four quartiles of salt intake. Participants taking angiotensin II receptor blocker (ARB) were 448, and mean systolic blood pressure in the four quartiles of salt intake were Q1:142.1 ± 17.7mmHg, Q2: 145.2 ± 17.3, Q3: 146.1 ± 17.2, and Q4: 147.8 ± 18.8. There was a stepwise increase in systolic blood pressure with increasing salt intake quartile (p = 0.018 for trend). Conclusions: For the elderly taking ARBs, salt reduction was shown to improve blood pressure control, but for the other elderly, no effect of salt intake was observed. Further studies are needed to examine including other factors what affects blood pressure for older population.

Association of Non-alcoholic Fatty Liver Disease With Salt Intake and Dietary Diversity in Chinese Medical Examination Adults Aged 18-59 Years: A Cross-Sectional Study.

ObjectivesGiven the significance of dietary factors in the development of non-alcoholic fatty liver disease (NAFLD). We conducted a cross-sectional study to investigate the association of NAFLD with salt intake and dietary diversity in a medical examination population aged 18–59 years.MethodsData from two Chinese health management centers were utilized between January 2017 and December 2019. The general information, laboratory tests, lifestyle habits, and diet of the participants were all evaluated. Based on alcohol consumption and abdominal ultrasound results, a total of 23,867 participants were divided into the NAFLD (n = 7,753) and control (n = 16,114) groups. Salt intake and dietary diversity were calculated separately for study participants using the spot urine method and dietary diversity scores (DDS). The multilevel logistic model and subgroup analysis were used to analyze the relationship between salt intake, dietary diversity, and NAFLD.ResultsWe found that the prevalence of NAFLD was 32.48%. Salt intake was associated with increased NAFLD (Q2 vs. Q1: OR = 1.201, 95% CI 1.094-1.317, P < 0.001; Q3 vs. Q1: OR = 1.442, 95% CI 1.316-1.580, P < 0.001; Q4 vs. Q1: OR = 1.604, 95% CI 1.465-1.757, P < 0.001), whereas sufficient dietary diversity was a protective factor for NAFLD (Sufficient DDS vs. Insufficient DDS: OR: 0.706, 95% CI 0.517-0.965, P < 0.05). The effects of salt intake and dietary diversity on NAFLD were equally stable in the subgroup analysis.ConclusionsWe can conclude that NAFLD is highly prevalent in medical examination adults aged 18-59 years in China. Furthermore, the risk of salt intake for NAFLD and the protective effect of dietary diversity on NAFLD should be taken into account in the management of NAFLD.

The association between salt intake and blood pressure is mediated by body mass index but modified by hypertension: The ELSA-Brasil study.

High salt intake has been linked to both obesity and high blood pressure (BP). Part of the variability of BP attributed to salt intake might be BMI-mediated. To investigate whether hypertension would be an effect modifier in the complex network including salt intake, obesity, and BP, we tested the hypothesis that salt intake has direct and BMI-mediated effects on systolic (SBP) and diastolic blood pressure (DBP). Data from 9,028 participants (aged 34-75 years, 53.6% women) were analyzed. A validated formula was used to estimate daily salt intake from the sodium excretion (12 h urine collection). A path model adjusted for covariates was designed in which salt intake has both a direct and a BMI-mediated effect on BP. In normotensives, standardized beta coefficients showed significant direct (Men: 0.058 and 0.052, Women: 0.072 and 0,061, P < 0.05) and BMI-mediated (Men: 0.040 and 0.065, Women: 0.038 and 0.067, P < 0.05) effect of salt intake on the SBP and DBP, respectively. However, in hypertensive individuals, neither the direct (Men: 0.006 and 0.056, Women: 0.048 and 0.017) nor the indirect effect (Men: -0.044 and 0.014, Women: 0.011 and 0.050) of salt intake on the SBP and DBP were significant. These data suggest that cardiovascular risk stratification should consider the complex interaction between salt intake and weight gain, and their effects on BP of normotensive and hypertensive individuals.

Effect of salt intake on clinical course and hemodynamics in patients with hypertrophic cardiomyopathy

Aim. To evaluate the relationship between the salt intake (NaCl) and the clinical and hemodynamic parameters in patients with hypertrophic cardiomyopathy (HCM).Material and methods. Forty four patients with HCM (mean age, 60,4±15,3 years) were examined. Particular attention was paid to intraventricular obstruction and hypovolemic syncope. NaCl consumption was estimated by 24-hour urine sodium test.Results. An inverse correlation was found between syncope and 24-hour natriuresis (r=-0,3, p=0,04). At 24-hour natriuresis &lt;50 mmol/day, syncope was more common (p=0,02): odds ratio (OR), 12,3 (95% confidence interval (CI): 1,3-121,3, p=0,03), as well as &lt;65 mmol/day (p=0,04): OR, 8,3 (95% CI: 1,13-60,3; p=0,04). At higher 24-hour urine sodium values, no reduction in syncope risk was recorded. A correlation was found between low values of left ventricular (LV) stroke volume index (SVI) (&lt;26 ml/m2) and 24-hour urine sodium (&lt;50 mmol/day) (r=0,5, p=0,01). An inverse correlation was observed between LV SVI and syncope at 24-hour natriuresis &lt;50 mmol/day (r=-0,9; p=0,05). An inverse relationship was found between the intraventricular obstruction and 24-hour urine sodium (r=-0,4, p=0,01). The prevalence of obstruction increased as natriuresis decreased: at 120 mmol/day, OR was 4,3 (95% CI: 1,01-18,6, p=0,048), at 110 mmol/day, OR — 4,6 (95% CI: 1,218,1, p=0,03), and at 100 mmol/day, OR — 4,0 (95% CI: 1,1-11,7, p=0,04). An increase in 24-hour urine sodium &gt;130 mmol/day was not followed by a further decrease in obstruction prevalence.Conclusion. To reduce the obstruction risk, the optimal 24-hour urine sodium level is ≥130 mmol/day (NaCl, 7,5 g/day). To reduce the syncope risk, regardless of obstruction presence, the optimal level of 24-hour natriuresis is ≥65 mmol/day (NaCl, 3,8 g/day).

Salt, but not protein intake, is associated with accelerated disease progression in autosomal dominant polycystic kidney disease

In autosomal dominant polycystic kidney disease (ADPKD), there are only scarce data on the effect of salt and protein intake on disease progression. Here we studied association of these dietary factors with the rate of disease progression in ADPKD and what the mediating factors are by analyzing an observational cohort of 589 patients with ADPKD. Salt and protein intake were estimated from 24-hour urine samples and the plasma copeptin concentration measured as a surrogate for vasopressin. The association of dietary intake with annual change in the estimated glomerular filtration rate (eGFR) and height adjusted total kidney volume (htTKV) growth was analyzed with mixed models. In case of significant associations, mediation analyses were performed to elucidate potential mechanisms. These patients (59% female) had a mean baseline age of 47, eGFR 64 mL/min/1.73m2 and the median htTKV was 880 mL. The mean estimated salt intake was 9.1 g/day and protein intake 84 g/day. During a median follow-up of 4.0 years, eGFR was assessed a median of six times and 24-hour urine was collected a median of five times. Salt intake was significantly associated with annual change in eGFR of-0.11 (95% confidence interval 0.20 --0.02] mL/min/1.73m2) per gram of salt, whereas protein intake was not (-0.00001 [-0.01 - 0.01] mL/min/1.73m2) per gram of protein). The effect of salt intake on eGFR slope was significantly mediated by plasma copeptin (crude analysis: 77% mediation, and, adjusted analysis: 45% mediation), but not by systolic blood pressure. Thus, higher salt, but not higher protein intake may be detrimental in ADPKD. The substantial mediation by plasma copeptin suggests that this effect is primarily a consequence of a salt-induced rise in vasopressin.

The effect of salt intake on the defensive strategies against inescapable innate fear and fear stress-associated learned despair in mice

The effect of salt intake on the defensive strategies against inescapable innate fear and fear stress-associated learned despair in mice

Effect of Salt Intake on the Serum Cardiotrophin-1 Levels in Chinese Adults

Background: Dietary sodium affects fluctuations in blood pressure (BP) and vascular function. Cardiotrophin-1 (CT-1), a stress-induced cytokine that belongs to the interleukin 6 family, is released by cells in response to potentially harmful stresses and plays a pivotal role in congestive heart failure, hypertension and arterial stiffness. In this study, we performed a randomized trial to confirm the effects of altered salt intake on the serum CT-1 levels in humans. Methods: Forty-four subjects (18–65 years of age) were selected from a rural community in northern China. All subjects initially maintained a baseline period for 3 days, transitioned to a low-salt (LS) diet for 7 days (3.0 g/day of NaCl) and then a high-salt (HS) diet for an additional 7 days (18.0 g/day of NaCl). Results: For the whole group, the serum CT-1 concentrations were significantly increased in the HS period compared to those of the LS period (293.50 ± 137.70 vs. 360.40 ± 162.83 pg/mL, p = 0.040). The serum CT-1 concentrations significantly decreased from the baseline period to the LS diet (419.91 ± 123.50 to 256.49 ± 109.75 pg/mL, p < 0.01) and significantly increased from the LS to HS diet (256.49 ± 109.75 to 414.39 ± 191.21 pg/mL, p < 0.01). These changes were observed in salt-sensitive (SS) individuals but not in salt-resistant (SR) individuals. In addition, a significant positive relationship was observed between the changes in the CT-1 concentrations and systolic BP as well as the changes in the mean arterial pressure from the LS period to the HS period (r = 0.376, p = 0.012; r = 0.311, p = 0.040). The serum CT-1 concentrations were positively correlated with the 24-h urinary sodium-to-potassium (Na/K) excretion ratios during both of the LS and HS diet intervention periods in SS subjects (r = 0.621, p < 0.01), but this correlation was not evident in SR subjects (r = 0.208, p = 0.107). Conclusions: Our study indicates that variations in dietary salt intake affect the serum CT-1 levels in Chinese adults.

A1461 Effect of salt intake on Plasma Urotensin II in Chinese subjects

A1461 Effect of salt intake on Plasma Urotensin II in Chinese subjects

A2633 Effect of Salt Intake on the Serum Cardiotrophin-1 Levels in Chinese Adults

A2633 Effect of Salt Intake on the Serum Cardiotrophin-1 Levels in Chinese Adults

Re-evaluation of the optimal cutoff of saline infusion test in the diagnosis of primary aldosteronism

Objective To assess the diagnostic value of saline infusion test (SIT) and its optimal cutoff in the diagnosis of primary aldosteronism (PA), and to analyze whether the dietary salt intake affects the SIT accuracy. Methods This is a prospective study. All 236 patients with a high risk for PA underwent the screening test, SIT and the fludrocortisone suppression test (FST) in separate days. The diagnosis of PA was established according to the FST criteria. According to the 24 h urinary sodium level, the patients were divided into low salt, normal salt, and high salt groups respectively, and the effect of salt intake on SIT was analyzed. Receiver operating characteristic (ROC) analysis was performed to compare the diagnostic accuracies. Results Finally, in 236 patients with high risk for PA, 134 patients with PA and 102 patients with essential hypertension (EH) were diagnosed. Using post-test plasma aldosterone concentration (PAC) for diagnosis, the area under the ROC curve (AUCROC) of the SIT was 0.974 (0.957, 0.991), which was significantly higher than that of the post-test plasma aldosterone to renin ratio (ARR) [0.900 (0.862, 0.938)] and that of the PAC suppression percentage [0.752 (0.690, 0.813)] (both P 0.05). Conclusion SIT is reliable for the diagnosis of PA. PAC post-SIT more than 8.0 ng/dl is recommended to confirm PA. (Chin J Endocrinol Metab, 2018, 34: 460-465) Key words: Primary aldosteronism; Saline infusion test; Sensitivity; Specificity

Effect of Salt Intake on Plasma and Urinary Uric Acid Levels in Chinese Adults: An Interventional Trial

Uric acid (UA) has been proposed as an important risk factor for cardiovascular and renal morbidity. We conducted an interventional trial to assess effects of altered salt intake on plasma and urine UA levels and the relationship between UA levels and salt sensitivity in humans. Ninety subjects (18–65 years old) were sequentially maintained on a normal diet for 3 days at baseline, a low-salt diet for 7 days (3.0 g/day, NaCl), and a high-salt diet for an additional 7 days (18.0 g/day of NaCl). Plasma UA levels significantly increased from baseline to low-salt diet and decreased from low-salt to high-salt diet. By contrast, daily urinary levels of UA significantly decreased from baseline to low-salt diet and increased from low-salt to high-salt diet. The 24 h urinary sodium excretions showed inverse correlation with plasma UA and positive correlation with urinary UA excretions. Additionally, salt-sensitive subjects presented significantly higher plasma UA changes in comparison to salt-resistant subjects, and a negative correlation was observed between degree of salt sensitivity and plasma UA difference. The present study indicates that variations in dietary salt intake affect plasma and urine UA levels, and plasma UA may be involved in pathophysiological process of salt sensitivity.

Effect of salt intake on afferent arteriolar dilatation: role of connecting tubule glomerular feedback (CTGF).

Afferent arteriole (Af-Art) resistance is modulated by two intrinsic nephron feedbacks: 1) the vasoconstrictor tubuloglomerular feedback (TGF) mediated by Na+-K+-2Cl- cotransporters (NKCC2) in the macula densa and blocked by furosemide and 2) the vasodilator connecting tubule glomerular feedback (CTGF), mediated by epithelial Na+ channels (ENaC) in the connecting tubule and blocked by benzamil. High salt intake reduces Af-Art vasoconstrictor ability in Dahl salt-sensitive rats (Dahl SS). Previously, we measured CTGF indirectly, by differences between TGF responses with and without CTGF inhibition. We recently developed a new method to measure CTGF more directly by simultaneously inhibiting NKCC2 and the Na+/H+ exchanger (NHE). We hypothesize that in vivo during simultaneous inhibition of NKCC2 and NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (PSF) in Dahl SS and that is enhanced with a high salt intake. In the presence of furosemide alone, increasing nephron perfusion did not change the PSF in either Dahl salt-resistant rats (Dahl SR) or Dahl SS. When furosemide and an NHE inhibitor, dimethylamiloride, were perfused simultaneously, an increase in tubular flow caused Af-Art dilatation that was demonstrated by an increase in PSF. This increase was greater in Dahl SS [4.5 ± 0.4 (SE) mmHg] than in Dahl SR (2.5 ± 0.3 mmHg; P < 0.01). We confirmed that CTGF causes this vasodilation, since benzamil completely blocked this effect. However, a high salt intake did not augment the Af-Art dilatation. We conclude that during simultaneous inhibition of NKCC2 and NHE in the nephron, CTGF induces Af-Art dilatation and a high salt intake failed to enhance this effect.

The Effect of Salt Intake and Potassium Supplementation on Serum Gastrin Levels in Chinese Adults: A Randomized Trial.

Excess dietary salt is strongly correlated with cardiovascular disease, morbidity, and mortality. Conversely, potassium likely elicits favorable effects against cardiovascular disorders. Gastrin, which is produced by the G-cells of the stomach and duodenum, can increase renal sodium excretion and regulate blood pressure by acting on the cholecystokinin B receptor. The aim of our study was to assess the effects of altered salt and potassium supplementation on serum gastrin levels in humans. A total of 44 subjects (38–65 years old) were selected from a rural community in northern China. All subjects were sequentially maintained on a relatively low-salt diet for 7 days (3.0 g/day of NaCl), a high-salt diet for 7 days (18.0 g/day of NaCl), and then a high-salt diet supplemented with potassium for another 7 days (18.0 g/day of NaCl + 4.5 g/day of KCl). The high-salt intake significantly increased serum gastrin levels (15.3 ± 0.3 vs. 17.6 ± 0.3 pmol/L). This phenomenon was alleviated through potassium supplementation (17.6 ± 0.3 vs. 16.5 ± 0.4 pmol/L). Further analyses revealed that serum gastrin was positively correlated with 24 h urinary sodium excretion (r = 0.476, p < 0.001). By contrast, gastrin level was negatively correlated with blood pressure in all dietary interventions (r = −0.188, p = 0.031). The present study indicated that variations in dietary salt and potassium supplementation affected the serum gastrin concentrations in the Chinese subjects.

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

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

Moderator's view: Salt, cardiovascular risk, observational research and recommendations for clinical practice.

In observational studies, blood pressure (BP), cholesterol and nutritional status biomarkers, including sodium intake, coherently show a J- or U-shaped relationship with health outcomes. Yet these data may reflect a stable sodium intake or a reduced intake due to comorbidities or intercurrent disease, or an intentional decrease in salt intake. Adjusting for comorbidities and risk factors may fail to eliminate confounding. For cholesterol and BP, we base our recommendations for prevention and treatment on interventional (experimental) studies. For sodium, we lack the perfect large-scale trial we would need, but substantial circumstantial information derived from interventional studies cannot be ignored. The objection that modelling the risk of salt excess for cardiovascular disease events based on the effect of salt intake on BP is unjustified fails to consider a recent meta-analysis showing that, independently of the intervention applied, intensive BP-lowering treatment (average BP 133/76 mmHg), compared with the less intensive treatment (140/81 mmHg), is associated with a 14% risk reduction for major cardiovascular events. In this knowledge context, inertia, i.e. awaiting the 'mother trial', is not justified. While recognizing that this trial may still be needed and that actual data, rather than modelled data, are the ideal solution, for now, the World Health Organization recommendation of reducing salt intake to <2 g/day of sodium (5 g/day of salt) in adults stands.

Effect of salt intake on beat-to-beat blood pressure nonlinear dynamics and entropy in salt-sensitive versus salt-protected rats

Blood pressure exhibits substantial short‐ and long‐term variability (BPV). We assessed the hypothesis that the complexity of beat‐to‐beat BPV will be differentially altered in salt‐sensitive hypertensive Dahl rats (SS) versus rats protected from salt‐induced hypertension (SSBN13) maintained on high‐salt versus low‐salt diet. Beat‐to‐beat systolic and diastolic BP series from nine SS and six SSBN13 rats (http://www.physionet.org) were analyzed following 9 weeks on low salt and repeated after 2 weeks on high salt. BP complexity was quantified by detrended fluctuation analysis (DFA), short‐ and long‐range scaling exponents (α S and α L), sample entropy (SampEn), and traditional standard deviation (SD) and coefficient of variation (CV(%)). Mean systolic and diastolic BP increased on high‐salt diet (P < 0.01) particularly for SS rats. SD and CV(%) were similar across groups irrespective of diet. Salt‐sensitive and ‐protected rats exhibited similar complexity indices on low‐salt diet. On high salt, (1) SS rats showed increased scaling exponents or smoother, systolic (P = 0.007 [α L]) and diastolic (P = 0.008 [α L]) BP series; (2) salt‐protected rats showed lower SampEn (less complex) systolic and diastolic BP (P = 0.046); and (3) compared to protected SSBN13 rats, SS showed higher α L for systolic (P = 0.01) and diastolic (P = 0.005) BP. Hypertensive SS rats are more susceptible to high salt with a greater rise in mean BP and reduced complexity. Comparable mean pressures in sensitive and protective rats when on low‐salt diet coupled with similar BPV dynamics suggest a protective role of low‐salt intake in hypertensive rats. This effect likely reflects better coupling of biologic oscillators.

Effects of salt intake and potassium supplementation on renalase expression in the kidneys of Dahl salt-sensitive rats.

Renalase is currently the only known amine oxidase in the blood that can metabolize catecholamines and regulate sympathetic activity. High salt intake is associated with high blood pressure (BP), possibly through the modulation of renalase expression and secretion, whereas potassium can reverse the high salt-mediated increase in blood pressure. However, whether potassium could also modulate BP through renalase is unclear. In this study, we aim to investigate how salt intake and potassium supplementation affect the level of renalase in rats. Eighteen salt-sensitive (SS) and 18 SS-13BN rats were divided into six groups, receiving normal salt (0.3% NaCl), high salt (8% NaCl) and high salt/potassium (8% NaCl and 8% KCl) dietary intervention for four weeks. At the end of experiments, blood and kidneys were collected for analysis. mRNA level of renalase was measured by quantitative real-time PCR and protein level was determined by Western blot. We found that mRNA and protein levels of renalase in the kidneys of SS and SS-13BN rats were significantly decreased (P < 0.05) after high salt intervention, whereas dopamine in plasma was increased (P < 0.05) compared with rats received normal salt, suggesting that salt may induce salt-sensitive hypertension through inhibition of renalase expression. We also found increased mRNA level and protein level of renalase, decreased catecholamine levels in plasma, and decreased BP in SS rats treated with high salt/potassium, compared with that of the high salt SS group. Taken together, the salt-induced increase and potassium-induced decrease in BP could be mediated through renalase. More studies are needed to confirm our findings and understand the underlying mechanisms.