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OBJECTIVES Hypertension phenotypes differ between Africans and Europeans, with a greater prevalence of low renin salt-sensitive hypertension and greater predisposition to adverse cardiac remodelling in Africans. To elucidate the roles of inheritance and environment in determining hypertension phenotypes in sub-Saharan Africans and white-Europeans, we compared phenotypes in white individuals in the UK (n = 132) and in African individuals in the UK (n = 158) and Nigeria (n = 179). METHODS Biochemistry, blood pressure, left ventricular structure (echocardiography) and 24-h urinary collections of sodium and potassium were measured. RESULTS Twenty-four-hour urinary sodium/potassium ratio was lower in individuals living in Europe (both African and white: 2.32 ± 0.15 and 2.28 ± 0.17) than in individuals in Nigeria (4.09 ± 0.26, both P

Reduced potassium (k+) intake has been linked to cardiovascular diseases. The underlying mechanisms remain unknown. Here, we investigate the effect of low (0%), normal (0.5%) and high K+ (5%) diet on the development of atherosclerosis and hypertensive cardiac damage. To induce atherosclerosis, apolipoprotein-deficient mice were infused with angiotensin (Ang) II (500ng/kg/min) for 28 days. Potassium treatment was initiated 2 weeks before Ang II infusion. Cardiac function was assessed by MRI. Levels of K+ in the serum and urine were significantly different between groups. The Ang II infused mice from the K+ low group had significantly higher atherosclerotic plaques in the aortic arch (21±3%) compared to K+ high (10±2%) and K+ normal (11±2%) groups. The atherosclerosis development was blood pressure independent since no differences in blood pressure between the groups were observed. Although heart to body-weight ratio did not differ between three groups, K+ low diet was associated with a lower ejection fraction rate and increased mRNA expression levels of cardiac ANP, BNP, collagen and fibronectin compared to the K+ normal and K+ high group. After Ang II infusion, assessment of aldosterone levels in urine showed significant higher aldosterone levels in the high K+ (214±72ng/24h) compared to normal K+ (26±6ng/24h) and low K+ (18±4ng/24h) groups. Aldosterone induced cardiovascular damage is known to be aggravated by sodium. To, evaluate whether high sodium diet unmask aldosterone mediated cardiovascular damage in the high K+ group, mice fed a high or normal K+ diet were additionally treated with high sodium (1% NaCl) in the drinking water. During Ang II treatment, high salt diet accelerated atherosclerosis in the aortic arch of both groups but no differences were observed between the high K+ high/high Na+ (41±7%) and normal K+/high Na+ (49±2%) group. In contrast, high K+/high Na+ group have significantly more severe cardiac hypertrophy compared to normal K+ high Na+ group (8.9±0.7 vs 6.4±0.7mg/g). These results were confirmed by MRI. K+ deficient diet induces atherosclerosis and cardiac damage during Ang II induced hypertension. K+ enriched diet exacerbates cardiac hypertrophy only under high Na+ conditions most likely in an aldosterone-dependent mechanism.

Introduction: Recently, the balance between sodium and potassium intake, i.e. sodium-to-potassium (Na/K) ratio, has received significant attention for prevention of hypertension. Previous studies reported the positive association between urinary Na/K (uNa/K) ratio and hypertension. However, even the same uNa/K ratio value, there might be high Na/ high K ratio or low Na/ low K ratio. Hypothesis: We assessed the hypothesis that blood pressure (BP) is higher in high Na/ high K group than that in low Na/ low K group even at the same uNa/K ratio in general population in cross-sectional study. Methods: The subjects were 20 to 74 years old who participated in The Tohoku Medical Megabank Project Community-based Cohort Study. Of these participants, we targeted 54,011 subjects (men: 20,505 women: 33,506 mean age: 59.9 years) who had information of BP, urinary Na and K. We estimated 24-h urinary excretion of Na and K using Tanaka formula. Urinary Na and K were each classified into quartiles (Na; Q1~Q4, K; Q1~Q4), and set all 16 groups of uNa/K ratio by combining Na and K respectively. To assess the relationship between casual uNa/K ratio and BP, we performed an analysis of covariance to calculate the adjusted mean systolic BP (SBP). We included covariate factors as age, sex, BMI and alcohol intake. We also assessed the relationship between uNa/K ratio and SBP using multiple regression analyses adjusted for covariate factors. We stratified the participants into two groups: ‘under treatment for hypertension’ (n=17,091) and ‘without treatment for hypertension (n=36,920)’. Results: The mean of uNa/K ratio for each group of Na (Q1)/K(Q1), Na (Q2)/K(Q2), Na (Q3)/K(Q3) and Na (Q4)/K(Q4) was all 4.0. As previous report showed, higher uNa/K ratio group showed higher SBP and lower uNa/K group showed lower BP. When we compared adjusted mean SBP of Na (Q1)/K(Q1) and Na (Q4)/K(Q4) the value were comparable, but the value were significantly higher in Na (Q4)/K(Q4) group (The adjusted mean SBP of Na (Q1)/K(Q1), Na (Q2)/K(Q2), Na (Q3)/K(Q3) and Na (Q4)/K(Q4) was 123.6, 124.9, 124.7 and 125.5 mmHg, respectively). The uNa/K was significantly positively associated with SBP independently of age, sex, BMI, and alcohol intake. The finding was unchanged the results in under treatment group. Conclusions: BP was significantly higher in high Na/ high K group than in low Na/ low K group even at the same uNa/K ratio. We suggested that not only increasing K intake but also reducing salt is important for preventing hypertension.

Increased intake of potassium should be promoted to reduce the risk of cardiovascular disease and stroke and to protect against bone loss, but confidence in recommended intakes depends on the strength of the evidence. All public health recommendations are considerably higher than current average intakes. Evidence on which current potassium intake recommendations for the United States, Europe, and globally have limitations. More recent evidence reviewed by the Agency for Healthcare Research and Quality affirms that more evidence is needed to define specific values for optimal potassium intakes. Potassium requirements undoubtedly vary with a number of factors including energy needs, race, and intake of sodium.

We have previously shown that systemic administration of (pro)renin receptor (PRR) decoy inhibitor PRO20 impaired kaliuretic response to high K + (HK) intake (5% KCl in diet). The present study extends this observation by examining the phenotype of inducible renal tubule-specific PRR knockout (RT PRR KO) mice fed a HK diet. The null mice were generated by breeding Floxed PRR mice with mice transgenic for Pax8-rtTA and LC-1 transgene. To induce RT PRR KO, mice with homozygous for Floxed PRR gene and hemizygous for the Pax8-rtTA and the LC-1 transgene were given 2 mg/ml doxycycline in 5% sucrose drinking water for 14 days followed by 4-wk off doxycycline. Following 1-wk HK intake, RT PRR KO mice had decreased urinary K + (by 33.6%) excretion and elevated plasma K + level (KO+HK: 5.38 ± 0.21 vs. Floxed+HK: 3.98 ± 0.03 mM, P + -K + -ATPase (160.3%), β-ENaC (130.2%), and cleaved-γ-ENaC (542.0%), and downregulated phosphorylated NCC-T53 (pNCC-T53) protein expression, all of which were significantly blunted in RT PRR KO mice (by 25-80%). In Flp-In T-REX 293 NCC cell line (stably expressing NCC), PRR siRNA significantly increased pNCC-T53 (by 72.3%) and partially reversed prorenin (100 nM)-induced inhibition of pNCC-T53 (by 38.2%). sPRR-His (10 nM) inhibited pNCC-T53 (by 48.9%), which were significantly reversed by losartan or angiotensin II receptor type 1 (AT1R) siRNA, without affecting total NCC expression. Together, these results suggest that PRR/sPRR contributes to the kaliuretic response through an impact on the intrarenal RAAS and the K + secretory machinery in the distal nephron.

Introduction: Recently, the balance between sodium and potassium intake, i.e. sodium-to-potassium (Na/K) ratio, has received a lot of attention for prevention of hypertension. Previous studies reported that the positive association between 24-hour urinary Na/K (uNa/K) ratio and hypertension. However, no studies have evaluated the relationship between uNa/K ratio measured by casual urine measurement and home hypertension in large populations. We aimed to clarify whether casual uNa/K ratio using the self-monitoring device was associated with home hypertension in general population. In addition, we assessed whether multiple days measurement of uNa/K ratio by casual urine increase the accuracy of the prediction of home hypertension compared with casual urine collected in a single day. Hypothesis: We assessed the hypothesis that multiple measurement of uNa/K ratio was positively associated with home hypertension, and increase the prediction of home hypertension compared with a single measurement. Methods: The subjects were over 20 years old who participated in The Tohoku Medical Megabank Project Cohort Study. Of these participants, we targeted 2,551 subjects who borrowed home blood pressure monitors (HEM-7080IC) and uNa/K ratio monitors (HEU-001F) for continuous 10 days. To assess the relationship between casual uNa/K ratio and home hypertension, we performed multiple logistic regression analyses and calculated aOR with 95% CI. We included covariate factors as age, sex, BMI and drinking status. In addition, to compare the prediction of home hypertension in multiple measurement with that in a single measurement, we calculated area under the ROC curve (AUROC) of uNa/K ratio. Home hypertension was defined as a SBP ≥ 135 mmHg and/or a DBP ≥ 85 mmHg. Results: Among 849 subjects had home hypertension (33.3%). Although uNa/K ratio was even positively associated with home hypertension by a single day (P for trend Conclusions: In conclusion, even single measurement of uNa/K ratio was positively associated with hypertension, the multiple measurement of uNa/K ratio strongly related with home hypertension. We suggested that multiple measurement of uNa/K ratio is desirable for assessing home hypertension because long term measurement of uNa/K ratio might reflect participants’ dietary balance of Na/K ratio.

Introduction: There is an association between dietary sodium/potassium intake and the pathogenesis of hypertension and cardiovascular disease. Some reports have indicated a correlation between psychological distress and high sodium intake. Victims who are affected by natural disasters tend to consume an unbalanced diet, with high sodium and low potassium levels, which may stem partly from high psychological distress due to natural disasters. Hypothesis: We tested the hypothesis that house collapse was associated with high urine Na/K (UNa/K) ratios in victims of the Great East Japan Earthquake. We also hypothesized that psychological distress could modify the relationship between house collapse and UNa/K ratio. Methods: We analyzed complete data collected from 24,580 coastal residents who did not take anti-hypertensive medications, were 20 to 74 years of age, and were enrolled in the Tohoku Medical Megabank Project Community-based Cohort (TMM CommCohort) Study. Participants were recruited between 2013 and 2015 at municipality-specific health checkup sites in the Iwate and Miyagi Prefectures. UNa/K ratios were assessed using spot urine samples. Participants were classified into four groups according to the extent of house collapse: total collapse (TC, n=4206); half collapse (HC, n=2825); partial collapse (PC, n=5964); and no damage (ND, n=11585). Using a covariance analysis, the multivariate-adjusted geometric means of the UNa/K ratios according to the group of house collapse were calculated, with adjustments for sex, age, systolic blood pressure, estimated glomerular filtration rate, HbA1c level, low-density lipoprotein cholesterol level, Kessler Psychological Distress Scale (K6) score, current alcohol consumption, current smoking habits, and daily exercise. In addition, after stratification according to K6 score (9/10), the multivariate-adjusted geometric means of the Una/K ratios were calculated according to house collapse group. Results: The multivariate-adjusted geometric means (95% confidence intervals) of UNa/K ratios of those whose houses underwent TC, HC, and PC were 3.33 (3.28-3.39), 3.37 (3.30-3.44), and 3.34 (3.30-3.40), respectively, all of which were significantly greater than the value of 3.23 (3.20-3.27) that was observed for the ND group. In analysis stratified by K6 score, the same tendencies were observed in both groups of K6 Conclusions: House collapse was significantly associated with high UNa/K ratios, and psychological distress did not modify this association.

Background: Increased potassium (K) intake has been reported to decrease blood pressure (BP) in animal studies as well as clinical trials. On this basis, major organizations including the American Heart Association recommend increasing K intake, preferably by diet, as a non pharmacological mean of reducing BP. However, it is not clear if the interventions for efficaciously increasing K intake are reproducible or feasible for translation into public health. Hence, we conducted a systematic review of the evidence to review this from randomized controlled trials (RCTs). Methods: We conducted a literature search using an information specialist of MEDLINE, EMBASE and Cochrane CENTRAL till November 2017. Two reviewers selected RCTs that were in adults, with an intervention aimed at increasing K intake, with blood pressure as an outcome. From RCTs which reported both a significant change in BP and K using 24 hour urine K, we evaluated the interventions for ease of reproducibility and feasibility based on prespecified criteria. Results: The initial search retrieved 1199 non-duplicate citations. After applying eligibility criteria, 90 studies were selected for inclusion. In 31 studies, the change in BP or K was not significant. Of the remaining 59 studies which reported a significant change in K and BP, 47 reported a change in K based on 24 hour urinary K measurement. 32/47 studies used a K supplement, with details provided on dose and administration to make it both reproducible and feasible. 15/47 studies used a dietary intervention, of which in 4, the intervention was not described in sufficient detail to be reproducible.The remaining 11 studies were feeding trials, with intervention consisting of provision of prepared meals, or of food items on a daily basis to make them unfeasible for routine clinical practice. Conclusions: Dietary potassium interventions from trials in which there was a significant change in K based on 24 hour urine and a significant change in BP are not reproducible or feasible.

Objective: Our aim was to analyze sodium and potassium intake in obese normotensive and hypertensive subjects from rural area. Design and method: Out of 1582 subjects (random rural sample) enrolled in ENAH study conducted in 2008–2010, 739 were invited for the second visit in 2015 and 377 subjects with reliable both urine samples (urine creatinine in normal ranges) were included in further analyses s (80m 297w ; average age 52 ± 13.5). Blood pressure was measured three times (Omron M6) and mean values were calculated. Fasting blood and first morning (spot) urine samples were collected. Sodium and potassium were determined using Tanaka, Kawasaki and Intersalt equations. Potassium intake was further adjusted for intestinal intake (77%) and renal excretion (92%). Optimal, normal, high normal BP, untreated and treated hypertension (HT) were diagnosed in 20.9%, 15.3%, 12.9%, 19.1% and 31.5%, respectively. There were 21.2%, 35.3% and 42.8% subjects in the BMI 1 (30) group, respectively. Results: Significant differences in HT prevalence were observed among the BMI groups (46.9%, 63.6%, 80 %, respectively ; p = 0.001). Sodium excretion were significantly lower in BMI1 vs BMI3 groups (BMI < 0.0001). More than 10 g/day of salt intake was most seldom present in BMI1 and more frequently in BMI3 group (41.9%, 54.5%, 63.1%, respectively ; p < 0.05). Compared to normotensive in hypertensive subjects salt intake >10 g/day was significantly more frequently presented in overweight (X2 = 12.68 ; p = 0.0003) but not in obese subjects. Potassium intake was significantly higher in BMI3 than in BMI1 group (p < 0.001). No differences in Na/K ratio were observed among BMI groups. Conclusions: Higher salt intake contributes to high prevalence of hypertension and according to our results is more closely associated with hypertension in overweight than in obese subjects. No difference in Na/K ratio among BMI groups reflects high sodium and poor potassium intake in all subjects.

See related article, pp 1083–1090 Hippocrates introduced personalized medicine >2500 years ago. He realized his patients were individuals and had to be assessed as such. The fact that one size does not fit all has been recognized by practicing physicians since that time. We automatically learn to phenotype our patients in terms of many criteria, in terms of age, sex, ethnic background, and numerous other classifications. Generally, no genetic testing necessary. In this month’s Hypertension , Shukri et al1 draw attention to several phenotypes. They studied a large number of normotensive and hypertensive men and women. The subjects ingested either a 200 or 10 mmol/d sodium diet with a generous and fixed potassium intake for 5 to 7 days. Angiotensin II (Ang II) infusions were performed at both sodium-intake levels, and aldosterone responses were monitored. The investigators found that women were more salt sensitive than men. The data showed a 30% greater degree of salt sensitivity in women, compared with men, irrespective of age or blood pressure status. Furthermore, with Ang II, the vascular, as reflected by change in renal blood …

Objective:Our aim was to analyze characteristics of subjects with new onset hypertension (NOHT) and impact of sodium and potassium intake on development of NOHT.Design and method:Out of 1582 subjects (random rural sample) enrolled in ENAH study conducted in 2008–2010, 739 were invited for the second

Objective:In Moldova, cardiovascular disease is the main cause of morbidity and mortality. High blood pressure is the leading risk factor for the CVD burden. It is common habit in Moldova to add salt to food at the table and when cooking and to eat processed food. The aim was to measure population s

Objective:Several national and international guideline groups recommend diets lower in sodium and higher in potassium, based on observational data demonstrating improved blood pressure and reduced cardiovascular risk. There is broad agreement that an event-based randomized clinical trial is needed t

To assess the effect of changing the sodium to potassium (Na/K) ratio on blood pressure at 4 years of follow-up. The measurements were carried out under identical conditions in two study periods (2008–2010 and 2012–2014). Urinary excretion of sodium and potassium (mmol/L) over 12 nocturnal hours was used to calculate the Na/K ratio and categorized by quintile. The 24-hour sodium and potassium intake was estimated using a validated equation. The mean BP was calculated from 3 measurements after 5 minutes of rest. Of the 15,105 participants at baseline, 14,014 completed the first follow-up. Participants without validated urine collection (n = 5,041), using antihypertensive medication (n = 3,860) at either time points or reporting bariatric surgery during follow-up (n = 45) were excluded. The differences between follow-up and baseline values were calculated for BP and the Na/K ratio. Analyses were stratified by sex and adjusted for confounding variables. Sodium intake did not change from baseline, but potassium intake increased by approximately 150 mg in both sexes (P

Objective:Excess salt (sodium chloride) and inadequate potassium intakes are responsible for high blood pressure in populations and they are associated with higher cardiovascular disease (CVD). In Montenegro, CVD is the leading cause of death and disability. Moreover, there is no survey that has dir

Previous studies have shown that a combination of avoidance conditioning schedules and increased intake of salt and water results in progressive hypertension in dogs within 14 days. The present experiments investigated the effects of increasing potassium intake upon blood pressure and heart rate of dogs made hypertensive by avoidance conditioning and salt-water loading. Two daily 30-minute sessions of free-operant avoidance conditioning were presented for 36 days during which isotonic saline was continuously infused into the arterial circulation (1.2 liters/day; 185 mEq Na+). Daily mean levels of systolic (22 +/- 5 mm Hg) and diastolic (12 +/- 4 mm Hg) pressure increased progressively in each dog during Days 1-14. Infusion of potassium chloride (100 mEq/day) from Days 15-28 resulted in progressive decreases in daily mean levels of systolic (-11 +/- 2 mm Hg) and diastolic (-8 +/- 1 mm Hg) pressure in each dog over this period. From Day 29-36, systolic (8 +/- 1 mm Hg) and diastolic (5 +/- 1 mm Hg) pressure increased. Normotensive dogs not on the avoidance schedule showed no change in arterial pressure in response to 14 days of potassium chloride infusion. These experiments show that the level of potassium, as well as sodium, intake significantly determines blood pressure levels in this form of experimental hypertension.

Nine well-motivated adults, knowledgeable about nutrition, kept food records, saved food portions equal to what had been eaten, and collected 24-hour urine samples for 3 consecutive days. Estimates of sodium and potassium intake were calculated from food table analyses of written food records and from flame photometric analyses of food portions. For each subject the mean of the estimates for each of the 3 days was compared with the mean of urine analyses for sodium and potassium for each of the 3 days. For the group of nine subjects, the average estimate of sodium intake from analyses of food records was 11% lower than the average estimate of urinary sodium excretion; the average estimate of sodium intake from analysis of food portions was 2% higher than urinary sodium excretion. For individuals, there were large differences between estimates of intake and measurement of sodium excretion. For the group of nine subjects, the average estimate of potassium intake from analysis of food records was less than 1% lower than the average estimate of potassium urinary excretion; the average estimate of potassium intake from analysis of food portions was 13% higher than potassium urinary excretion. For individuals, as with sodium, there were large differences between estimates of intake and measurement of potassium excretion.

These studies examine the effect of sodium (Na) and potassium (K) intake on the pressor and metabolic actions of ACTH (20 micrograms/kg/day) in sheep. After 21 days on each of five regimens in which Na and K intake varied from 0 to 100 mmol/day, no simple relationship between Na and K intake and blood pressure was found. After five days of ACTH treatment, mean arterial pressure (MAP) rose + 5 mmHg in sheep on 0 mmol Na, 0 mmol K (expressed as 0 Na 0 K); + 13 mmHg on 10 Na 100 K; + 5 mmHg on 0 Na 100 K; + 20 mmHg on 100 Na 0 K and + 24 mmHg on 100 Na 100 K. Plasma [K] was unchanged by ACTH on 0 Na 0 K but fell in sheep on the other electrolyte regimens. Water intake increased with ACTH on all regimens except 100 Na 0 K. Blood aldosterone concentration was high in sheep maintained on 0 Na regimens but lower after five days of ACTH treatment in all groups. Blood cortisol and corticosterone concentrations increased with ACTH on all regimens studied.