Dietary sodium affects systemic and renal hemodynamic response to NO inhibition in healthy humans

1998 ◽  
Vol 274 (5) ◽  
pp. F914-F923 ◽  
Author(s):  
J. N. Bech ◽  
C. B. Nielsen ◽  
P. Ivarsen ◽  
K. T. Jensen ◽  
E. B. Pedersen
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Hemodynamics ◽  
Dietary Sodium ◽  
High Sodium ◽  
High Sodium Intake ◽  
Healthy Humans ◽  
Low Sodium ◽  
Arterial Blood ◽  
Relative Decrease

Animal studies have indicated that increased nitric oxide (NO) synthesis plays a significant role in the renal adaptation to increased sodium intake. To investigate the role of NO during increased sodium intake in humans, we studied the effect of acute, systemic injection of N G-monomethyl-l-arginine (l-NMMA) on renal hemodynamics [glomerular filtration rate and renal plasma flow (GFR and RPF, respectively)], urinary sodium excretion (FENa), systemic hemodynamics [mean arterial blood pressure and heart rate (MAP and HR)], and plasma levels of several vasoactive hormones in 12 healthy subjects during high (250 mmol/day) and low (77 mmol/day) sodium intake in a crossover design. The sodium diets were administered for 5 days before the l-NMMA treatments, in randomized order, with a washout period of 9 days between each diet and l-NMMA treatment. GFR and RPF were measured using the renal clearance of51Cr-labeled EDTA and125I-labeled hippuran by the constant infusion technique in clearance periods of 30-min duration. Two baseline periods were obtained, after whichl-NMMA was given (3 mg/kg over 10 min), and the effect of treatment was followed over the next five clearance periods. During high sodium intake,l-NMMA induced a more pronounced relative decrease in RPF ( P = 0.0417, ANOVA), a more pronounced relative decrease in FENa( P = 0.0032, ANOVA), and a more pronounced relative increase in MAP ( P= 0.0231, ANOVA). During low sodium intake, the effect ofl-NMMA on FENa was abolished. During low sodium intake, l-NMMA induced a sustained drop in plasma renin (31 ± 5 vs. 25 ± 5 μU/ml, P < 0.001), which was not seen during high sodium intake. The data indicate that increased production of NO is an important part of the adaptation to increased dietary sodium intake in healthy humans, with respect to renal hemodynamics, sodium excretion, and the secretion of renin.

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis

2002 ◽  
Vol 92 (5) ◽  
pp. 2097-2104 ◽  
Author(s):  
Claudia Höhne ◽  
Willehad Boemke ◽  
Nora Schleyer ◽  
Roland C. Francis ◽  
Martin O. Krebs ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Respiratory Alkalosis ◽  
High Sodium ◽  
Low Sodium ◽  
Oxygen Fraction ◽  
Arterial Blood ◽  
Inspiratory Oxygen

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium · kg body wt−1 · day−1) or high-sodium (HS = 7.5 mmol sodium · kg body wt−1 · day−1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial Po 2 34.4 ± 2.1 Torr), plasma pH increased from 7.37 ± 0.01 to 7.48 ± 0.01 ( P < 0.05) because of hyperventilation (arterial Pco 2 25.6 ± 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

P4540Obesity in patients with heart failure and without diabetes mellitus is associated with longer event-free survival only among those with high dietary sodium intake

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Z Saleh ◽  
T Lennie ◽  
D Moser
Keyword(s):  
Diabetes Mellitus ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Obese Patients ◽  
Event Free Survival ◽  
Free Survival ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium ◽  
Patients With Heart Failure

Abstract Background Obesity is paradoxically associated with better short- and long-term outcomes in patients with heart failure (HF) and without diabetes mellitus (DM). While excessive dietary sodium intake is common among obese persons, its impact on the association between obesity and outcomes has not been considered. Aim To determine whether dietary sodium intake levels would affect the association between obesity and better outcomes in patients with HF and without DM. Method A sample of 129 patients (age 60±12.4 years; 30% female) provided a single 24-hour urine collection sample to estimate dietary sodium intake. Patients were divided into 4 groups based on body mass index (BMI) and the sodium intake recommendation for HF of 3g/day (obese with high sodium intake [n=41; 32%], obese with low sodium intake [n=16; 12%], non-obese with high sodium intake [n=35; 27%], and non-obese with low sodium intake [n=37; 29%]). Patients were followed-up during an average period of 395 days to determine time to first event of all-cause hospitalization or death. Cox regression was used to determine the association between obesity and outcomes in the context of sodium intake after controlling for age, gender, NYHA class (I II vs. III IV) and LVEF. Results There were 41 patients (31.8%) who had an event of all-cause hospitalization or death. Obese patients with high sodium intake had 61% lower risk for events than those non-obese with low dietary sodium intake (figure). There were no differences in the event-free survival among other groups. Conclusion These data suggest that dietary sodium intake may be particularly important for obese patients with HF and without DM.

scholarly journals Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake–Induced Modulation of Na-Cl Cotransporter

2018 ◽  
Vol 30 (2) ◽  
pp. 216-227 ◽  
Author(s):  
Peng Wu ◽  
Zhong-Xiuzi Gao ◽  
Xiao-Tong Su ◽  
Ming-Xiao Wang ◽  
Wen-Hui Wang ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Knockout Mice ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Wild Type ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium ◽  
Inwardly Rectifying Potassium Channel ◽  
Urinary Potassium

BackgroundDietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT). Whether the basolateral, inwardly rectifying potassium channel Kir4.1/Kir5.1 (a heterotetramer of Kir4.1/Kir5.1) in the DCT is essential for mediating the effect of dietary sodium intake on NCC activity is unknown.MethodsWe used electrophysiology, renal clearance techniques, and immunoblotting to examine effects of Kir4.1/Kir5.1 in the DCT and NCC in wild-type and kidney-specific Kir4.1 knockout mice.ResultsLow sodium intake stimulated basolateral Kir4.1/Kir5.1 activity, increased basolateral K+ conductance, and hyperpolarized the membrane. Conversely, high sodium intake inhibited the potassium channel, decreased basolateral K+ currents, and depolarized the membrane. Low sodium intake increased total and phosphorylated NCC expression and augmented hydrochlorothiazide-induced natriuresis; high sodium intake had opposite effects. Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. In contrast, dietary sodium intake did not affect NCC activity in knockout mice. Further, Kir4.1 deletion not only abolished basolateral K+ conductance and depolarized the DCT membrane, but also abrogated the stimulating effects induced by low sodium intake on basolateral K+ conductance and hyperpolarization. Finally, dietary sodium intake did not alter urinary potassium excretion rate in hypokalemic knockout and wild-type mice.ConclusionsStimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC.

Impact of high sodium intake on blood pressure and functional sympatholysis during rhythmic handgrip exercise

2020 ◽  
Vol 45 (6) ◽  
pp. 613-620
Author(s):  
Jacob T. Caldwell ◽  
Shelbi L. Sutterfield ◽  
Hunter K. Post ◽  
Garrett M. Lovoy ◽  
Heather R. Banister ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brachial Artery ◽  
Sodium Intake ◽  
Cardiovascular Responses ◽  
Dietary Sodium ◽  
Handgrip Exercise ◽  
High Sodium ◽  
High Sodium Intake ◽  
Healthy Humans ◽  
Functional Sympatholysis

High dietary sodium intake is a risk factor for arterial hypertension; given that the ability to overcome sympathetically mediated vasoconstriction (functional sympatholysis) is attenuated in individuals with hypertension, we investigated the cardiovascular responses to high salt (HS) intake in healthy humans. We hypothesized that a HS intake of 15 g/day for 7 days would attenuate functional sympatholysis and augment the blood pressure response to handgrip exercise (HGE). Thirteen participants (6 males, 7 females) underwent 2 individual days of testing. Beat-by-beat blood pressure and heart rate were recorded throughout the trial on the non-exercising limb. Forearm blood flow was derived from ultrasonography on the brachial artery of the exercising limb. Participants then underwent a flow-mediated dilation (FMD) test. Next, a submaximal HGE was performed for 7 min with lower body negative pressure initiated during minutes 5–7. A single spot urine sample revealed a significant increase in sodium excretion during the HS conditions (p < 0.01). FMD was reduced during the HS condition. Mean arterial pressure was significantly higher during HS intake. No alteration to functional sympatholysis was found between conditions (p > 0.05). In summary, HS intake increases blood pressure without impacting functional sympatholysis or blood pressure responsiveness during HGE. These findings indicate that brachial artery dysfunction precedes an inefficient functional sympatholysis. Novelty Functional sympatholysis was not impacted by 1 week of high sodium intake. High sodium intake augmented the rate pressure product during handgrip exercise in healthy humans.

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

2008 ◽  
Vol 294 (1) ◽  
pp. R17-R25 ◽  
Author(s):  
Mads Kjolby ◽  
Peter Bie
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Low Sodium ◽  
Arterial Blood ◽  
Body Sodium ◽  
Custom Made ◽  
Total Body

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03–0.75 mmol·kg−1·day−1for 7 days. Acute NaCl administration increased PV (+6.3–8.9%) and plasma sodium concentration (∼2%) and decreased plasma protein concentration (−6.4–8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.

scholarly journals Dietary Sodium Intake and Risk of Cardiovascular Disease: A Systematic Review and Dose-Response Meta-Analysis

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2934
Author(s):  
Yi-Jie Wang ◽  
Tzu-Lin Yeh ◽  
Ming-Chieh Shih ◽  
Yu-Kang Tu ◽  
Kuo-Liong Chien
Keyword(s):  
Cardiovascular Disease ◽  
Dose Response ◽  
Disease Risk ◽  
Sodium Intake ◽  
Meta Analysis ◽  
Cardiovascular Disease Risk ◽  
Dietary Sodium ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium

Dietary sodium intake has received considerable attention as a potential risk factor of cardiovascular disease. However, evidence on the dose-response association between dietary sodium intake and cardiovascular disease risk is unclear. Embase and PubMed were searched from their inception to 17 August 2020 and studies that examined the association between sodium intake and cardiovascular disease in adolescents were not included in this review. We conducted a meta-analysis to estimate the effect of high sodium intake using a random effects model. The Newcastle-Ottawa Scale assessment was performed. A random-effects dose-response model was used to estimate the linear and nonlinear dose-response relationships. Subgroup analyses and meta-regression were conducted to explain the observed heterogeneity. We identified 36 reports, which included a total of 616,905 participants, and 20 of these reports were also used for a dose-response meta-analysis. Compared with individuals with low sodium intake, individuals with high sodium intake had a higher adjusted risk of cardiovascular disease (Rate ratio: 1.19, 95% confidence intervals = 1.08–1.30). Our findings suggest that there is a significant linear relationship between dietary sodium intake and cardiovascular disease risk. The risk of cardiovascular disease increased up to 6% for every 1 g increase in dietary sodium intake. A low-sodium diet should be encouraged and education regarding reduced sodium intake should be provided.

scholarly journals Is socio-demographic status, body mass index, and consumption of food away from home associated with high sodium intake among adults in Malaysia?: findings from the Malaysian Community Salt Survey (MyCoSS)

2021 ◽  
Vol 40 (S1) ◽  
Author(s):  
Ruhaya Salleh ◽  
Shubash Shander Ganapathy ◽  
Norazizah Ibrahim Wong ◽  
Siew Man Cheong ◽  
Mohamad Hasnan Ahmad ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Logistic Regression ◽  
Body Mass ◽  
Sodium Intake ◽  
Daily Intake ◽  
Dietary Sodium ◽  
Cooking Methods ◽  
High Sodium ◽  
High Sodium Intake ◽  
Meal Consumption

Abstract Background Studies have shown that having away from home meals contributes to high sodium intake among young people and those who lived in urban areas. This study aimed to determine the association between dietary sodium intake, body mass index, and away from home meal consumption behaviour among Malaysian adults. Methods MyCoSS was a cross-sectional household survey involving 1440 adults age 18 years and above. This study utilized stratified cluster sampling to obtain a nationally representative sample. Data was collected between October 2017 and March 2018. Socio-demographic information, dietary assessment using food frequency questionnaire (FFQ), and away from home meal consumption were assessed through a face-to-face interview by trained health personnel. Descriptive analysis and logistic regression were applied to identify the association of socioeconomic status and away from home meal consumption with dietary sodium intake. Results A total of 1032 participants completed the FFQ, with a mean age of 48.8 + 15.6 years. Based on the FFQ, slightly over half of the participants (52.1%) had high sodium intake. Results showed that 43.6% of participants consumed at least one to two away from home meals per day, while 20.8% of them had their three main meals away from home. Participants aged less than 30 years old were the strongest predictor to consume more sodium (adjusted OR: 3.83; 95%CI: 2.23, 6.58) while those of Indian ethnicity had significantly lower sodium intake. Surprisingly, having three away from home meals per day was not associated with high dietary sodium intake, although a significant association (crude OR; 1.67, 95% CI: 1.19, 2.35) was found in the simple logistic regression. Obese participants were less likely to have high dietary sodium intake compared with the normal BMI participants in the final model. Conclusion Over half of the participants consumed sodium more than the recommended daily intake, especially those who consumed three away from home meals. However, there was no significant association between high sodium intake and having three away from home meals per day. The promotion of healthy cooking methods among the public must continue to be emphasized to reduce the dietary sodium intake among Malaysian adults.

Renal and cardiac oxidative/nitrosative stress in salt-loaded pregnant rat

2007 ◽  
Vol 293 (4) ◽  
pp. R1657-R1665 ◽  
Author(s):  
Annie Beauséjour ◽  
Véronique Houde ◽  
Karine Bibeau ◽  
Rébecca Gaudet ◽  
Jean St-Louis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitrosative Stress ◽  
Gestational Hypertension ◽  
Sodium Intake ◽  
Pregnant Rats ◽  
High Sodium ◽  
High Sodium Intake ◽  
Arterial Blood ◽  
Cardiac Ventricle

Sodium supplementation given for 1 wk to nonpregnant rats induces changes that are adequate to maintain renal and circulatory homeostasis as well as arterial blood pressure. However, in pregnant rats, proteinuria, fetal growth restriction, and placental oxidative stress are observed. Moreover, the decrease in blood pressure and expansion of circulatory volume, normally associated with pregnancy, are prevented by high-sodium intake. We hypothesized that, in these pregnant rats, a loss of the balance between prooxidation and antioxidation, particularly in kidneys and heart, disturbs the normal course of pregnancy and leads to manifestations such as gestational hypertension. We thus investigated the presence of oxidative/nitrosative stress in heart and kidneys following high-sodium intake in pregnant rats. Markers of this stress [8-isoprostaglandin F2α (8-iso-PGF2α) and nitrotyrosine], producer of nitric oxide [nitric oxide synthases (NOSs)], and antioxidants [superoxide dismutase (SOD) and catalase] were measured. Then, molecules (Na+-K+-ATPase and aconitase) or process [apoptosis (Bax and Bcl-2), inflammation (monocyte chemoattractant protein-1, connective tissue growth factor, and TNF-α)] susceptible to free radicals was determined. In kidneys from pregnant rats on 1.8% NaCl-water, NOSs, apoptotic index, and nitrotyrosine expression were increased, whereas Na+-K+-ATPase mRNA and activity were decreased. In the left cardiac ventricle of these rats, heightened nitrotyrosine, 8-iso-PGF2α, and catalase activity together with reduced endothelial NOS protein expression and SOD and aconitase activities were observed. These findings suggest that oxidative/nitrosative stress in kidney and left cardiac ventricle destabilizes the normal course of pregnancy and could lead to gestational hypertension.

scholarly journals Sodium Sensitivity, Sodium Resistance, and Incidence of Hypertension

Hypertension ◽  
2021 ◽  
Author(s):  
Jiang He ◽  
Jian-Feng Huang ◽  
Changwei Li ◽  
Jing Chen ◽  
Xiangfeng Lu ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Experimental Studies ◽  
Dietary Sodium ◽  
Cross Sectional ◽  
Incident Hypertension ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
Sodium Diet ◽  
Low Sodium ◽  
Increased Risk

Cross-sectional studies have reported that high sodium sensitivity is more common among individuals with hypertension. Experimental studies have also reported various animal models with sodium-resistant hypertension. It is unknown, however, whether sodium sensitivity and resistance precede the development of hypertension. We conducted a feeding study, including a 7-day low-sodium diet (1180 mg/day) followed by a 7-day high-sodium diet (7081 mg/day), among 1718 Chinese adults with blood pressure (BP) <140/90 mm Hg. We longitudinally followed them over an average of 7.4 years. Three BP measurements and 24-hour urinary sodium excretion were obtained on each of 3 days during baseline observation, low-sodium and high-sodium interventions, and 2 follow-up studies. Three trajectories of BP responses to dietary sodium intake were identified using latent trajectory analysis. Mean (SD) changes in systolic BP were −13.7 (5.5), −4.9 (3.0), and 2.4 (3.0) mm Hg during the low-sodium intervention and 11.2 (5.3), 4.4 (4.1), and −0.2 (4.1) mm Hg during the high-sodium intervention ( P <0.001 for group differences) in high sodium-sensitive, moderate sodium-sensitive, and sodium-resistant groups, respectively. Compared with individuals with moderate sodium sensitivity, multiple-adjusted odds ratios (95% CIs) for incident hypertension were 1.43 (1.03–1.98) for those with high sodium sensitivity and 1.43 (1.03–1.99) for those with sodium resistance ( P =0.006 for nonlinear trend). Furthermore, a J-shaped association between systolic BP responses to sodium intake and incident hypertension was identified ( P <0.001). Similar results were observed for diastolic BP. Our study indicates that individuals with either high sodium sensitivity or sodium resistance are at an increased risk for developing hypertension.

scholarly journals Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study

BMJ ◽  
2019 ◽  
pp. l772 ◽  
Author(s):  
Martin O’Donnell ◽  
Andrew Mente ◽  
Sumathy Rangarajan ◽  
Matthew J McQueen ◽  
Neil O’Leary ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Cardiovascular Events ◽  
Sodium Intake ◽  
Urinary Sodium ◽  
Potassium Excretion ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium ◽  
Sodium And Potassium

AbstractObjectiveTo evaluate the joint association of sodium and potassium urinary excretion (as surrogate measures of intake) with cardiovascular events and mortality, in the context of current World Health Organization recommendations for daily intake (<2.0 g sodium, >3.5 g potassium) in adults.DesignInternational prospective cohort study.Setting18 high, middle, and low income countries, sampled from urban and rural communities.Participants103 570 people who provided morning fasting urine samples.Main outcome measuresAssociation of estimated 24 hour urinary sodium and potassium excretion (surrogates for intake) with all cause mortality and major cardiovascular events, using multivariable Cox regression. A six category variable for joint sodium and potassium was generated: sodium excretion (low (<3 g/day), moderate (3-5 g/day), and high (>5 g/day) sodium intakes) by potassium excretion (greater/equal or less than median 2.1 g/day).ResultsMean estimated sodium and potassium urinary excretion were 4.93 g/day and 2.12 g/day, respectively. After a median follow-up of 8.2 years, 7884 (6.1%) participants had died or experienced a major cardiovascular event. Increasing urinary sodium excretion was positively associated with increasing potassium excretion (unadjusted r=0.34), and only 0.002% had a concomitant urinary excretion of <2.0 g/day of sodium and >3.5 g/day of potassium. A J-shaped association was observed of sodium excretion and inverse association of potassium excretion with death and cardiovascular events. For joint sodium and potassium excretion categories, the lowest risk of death and cardiovascular events occurred in the group with moderate sodium excretion (3-5 g/day) and higher potassium excretion (21.9% of cohort). Compared with this reference group, the combinations of low potassium with low sodium excretion (hazard ratio 1.23, 1.11 to 1.37; 7.4% of cohort) and low potassium with high sodium excretion (1.21, 1.11 to 1.32; 13.8% of cohort) were associated with the highest risk, followed by low sodium excretion (1.19, 1.02 to 1.38; 3.3% of cohort) and high sodium excretion (1.10, 1.02 to 1.18; 29.6% of cohort) among those with potassium excretion greater than the median. Higher potassium excretion attenuated the increased cardiovascular risk associated with high sodium excretion (P for interaction=0.007).ConclusionsThese findings suggest that the simultaneous target of low sodium intake (<2 g/day) with high potassium intake (>3.5 g/day) is extremely uncommon. Combined moderate sodium intake (3-5 g/day) with high potassium intake is associated with the lowest risk of mortality and cardiovascular events.

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