Short-Term RCT of Increased Dietary Potassium from Potato or Potassium Gluconate: Effect on Blood Pressure, Microcirculation, and Potassium and Sodium Retention in Pre-Hypertensive-to-Hypertensive Adults.
Ontology highlight
ABSTRACT:
SUBMITTER: Stone MS
PROVIDER: S-EPMC8151047 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Potassium supplementation has been associated with reduced urinary calcium (Ca) excretion and increased Ca balance. Dietary interventions assessing the impact of potassium on bone are lacking. In this secondary analysis of a study designed primarily to determine blood pressure effects, we assessed the effects of potassium intake from potato sources and a potassium supplement on urinary Ca, urine pH, and Ca balance. Thirty men (n = 15) and women (n = 15) with a mean ± SD age and BMI of 48.2 ± 15 years and 31.4 ± 6.1 kg/m2, respectively, were enrolled in a cross-over, randomized control feeding trial. Participants were assigned to a random order of four 16-day dietary potassium interventions including a basal diet (control) of 2300 mg/day (~60 mmol/day) of potassium, and three phases of an additional 1000 mg/day (3300 mg/day(~85 mmol/day) total) of potassium in the form of potatoes (baked, boiled, or pan-heated), French fries (FF), or a potassium (K)-gluconate supplement. Calcium intake for all diets was approximately 700-800 mg/day. Using a mixed model ANOVA there was a significantly lower urinary Ca excretion in the K-gluconate phase (96 ± 10 mg/day) compared to the control (115 ± 10 mg/day; p = 0.027) and potato (114 ± 10 mg/day; p = 0.033). In addition, there was a significant difference in urinary pH between the supplement and control phases (6.54 ± 0.16 vs. 6.08 ± 0.18; p = 0.0036). There were no significant differences in Ca retention. An increased potassium intake via K-gluconate supplementation may favorably influence urinary Ca excretion and urine pH. This trial was registered at ClinicalTrials.gov as NCT02697708.
| S-EPMC8707887 | biostudies-literature
Project description:PurposeOCT-angiography (OCT-A) offers a non-invasive method to visualize retinochoroidal microvasculature. As glaucoma disease affects retinal ganglion cells in the macula, macular microcirculation is of interest. The purpose of the study was to investigate regional macular vascular characteristics in patients with ocular hypertension (OHT), pre-perimetric primary open-angle glaucoma (pre-POAG) and controls by OCT-A in three microvascular layers.Material and methods180 subjects were recruited from the Erlangen Glaucoma Registry, the Department of Ophthalmology, University of Erlangen and residents: 38 OHT, 20 pre-POAG, 122 controls. All subjects received an ophthalmological examination including measurements of retinal nerve fibre layer (RNFL), retinal ganglion cell layer (RGC), inner nuclear layer (INL), and Bruch's Membrane Opening-Minimum Rim Width (BMO-MRW). Macular vascular characteristics (vessel density, VD, foveal avascular zone, FAZ) were measured by OCT-A (Spectralis OCT II) in superficial vascular plexus (SVP), intermediate capillary plexus (ICP), and deep capillary plexus (DCP).ResultsWith age correction of VD data, type 3 tests on fixed effects showed a significant interaction between diagnosis and sectorial VD in SVP (p = 0.0004), ICP (p = 0.0073), and DCP (p = 0.0003). Moreover, a significance in sectorial VD was observed within each layer (p<0.0001) and for the covariate age (p<0.0001). FAZ differed significantly between patients' groups only in ICP (p = 0.03), not in SVP and DCP. For VD the AUC values of SVP, ICP, and DCP were highest among diagnostic modalities (AUC: 0.88, 95%-CI: 0.75-1.0, p<0.001).ConclusionRegional reduced macula VD was observed in all three retinal vascular layers of eyes with OHT and pre-POAG compared to controls, indicating localized microvascular changes as early marker in glaucoma pathogenesis.
| S-EPMC7877568 | biostudies-literature
Project description:High dietary sodium and low potassium intake increase blood pressure and risk of hypertension, but whether the relationship between dietary sodium and potassium and risk of hypertension is different in North China and South China remains unclear. We used data from the longitudinal China Health and Nutrition Survey (CHNS) and selected 6705 adults who participated in at least two waves in 2009, 2011, and 2015 and had no hypertension in baseline. We performed multiple linear regression analysis and multiple logistic regressions stratified by area for the present study design. Sodium and potassium intake were higher in North China (4343.4 and 1624.8 mg/day, respectively) than in South China (4107.8 and 1516.1 mg/d, respectively) (p < 0.05). Multiple linear regression revealed that a positive correlation of sodium intake (? = 0.026, p < 0.05) and ratio of sodium to potassium (Na-K) intake (? = 0.041, p < 0.01) with diastolic blood pressure (DBP) was found in North China, and the association of sodium, potassium, and Na-K intake ratio with blood pressure was different in South China. Multiple logistic regressions documented a similar significant inverse association between dietary potassium intake and risk of hypertension in both North China and South China (risk ratio (RR): 0.63, 95%CI: 0.50-0.79; RR: 0.80, 95%CI: 0.66-0.98, respectively). The risk of hypertension increased in the fourth quartile of dietary sodium and Na-K intake ratio (RR: 1.20, 95%CI: 1.00-1.44; RR: 1.35, 95%CI: 1.13-1.62, respectively) in North China but no association was observed in South China. The current study indicates a different association of dietary sodium and Na-K intake ratio with systolic blood pressure (SBP), DBP, and risk of hypertension in North China and South China.
| S-EPMC7071283 | biostudies-literature
Project description:BACKGROUND:To explore how central hemodynamics respond to dietary sodium and potassium interventions, and whether the responses are associated with metabolic traits. METHODS:We conducted a dietary intervention study including a 7-day low-sodium (51.3 mmol sodium/day) intervention, a 7-day high-sodium (307.8 mmol sodium/day) intervention, and a 7-day high-sodium with potassium supplementation (60.0 mmol potassium/day) intervention among 99 northern Chinese subjects aged 18-60 years. Five metabolic traits included abdominal obesity, high triglycerides, low HDL cholesterol, raised blood pressure (BP), and high glucose. Central hemodynamics were measured at baseline and during each intervention. RESULTS:Central systolic BP (SBP), diastolic BP (DBP), pulse pressure (PP), and augmentation index (AIx@75) significantly decreased during low-sodium intervention, increased during high-sodium intervention, and then decreased during potassium supplementation. We observed potential linear trends toward significance of central SBP and PP responses to low-sodium intervention, and significant linear trends of responses to high-sodium intervention as the number of metabolic traits grows. For example, among participants with 0 or 1, 2 or 3, and 4 or 5 metabolic traits, central SBP responses to high-sodium intervention were 8.8 [95% confidence interval (5.8, 11.8)], 9.3 (7.1, 11.6), and 14.0 (11.6, 16.3) mmHg, respectively (P for trend = 0.009). Significant linear trends of central SBP and DBP responses to potassium supplementation were also observed. CONCLUSIONS:Central BP and AIx@75 were lowered by sodium reduction and potassium supplementation, and elevated by sodium-loading. The responses of central BP were pronounced among individuals with metabolic traits clustering. CLINICAL TRIALS REGISTRATION:Trial Number NCT00721721 (The current study is registered on ClinicalTrials.gov; https://clinicaltrials.gov).
| S-EPMC6887692 | biostudies-literature
Project description:The influence of dietary sodium and potassium on blood pressure (BP) has been extensively studied, however their impact on endothelial function, particularly any interactive effects, has received less attention. The purpose of this study was to determine if dietary potassium can offset the deleterious effect of high dietary sodium on endothelial function independent of BP. Thirty-three adults with salt-resistant BP (16 M and 17 F; 27 ± 1 year) completed seven days each of the following diets in a random order: a moderate potassium/low sodium diet (65 mmol potassium/50 mmol sodium; MK/LS), a moderate potassium/high sodium diet (65mmol potassium/300 mmol sodium; MK/HS) and a high potassium/high sodium (120 mmol potassium/300 mmol sodium; HK/HS). On day seven of each diet, 24-h ambulatory BP and a urine collection were performed. Brachial artery flow-mediated dilation (FMD) was measured in response to reactive hyperemia. Between diets, 24-h BP was unchanged confirming salt resistance (p > 0.05). Sodium excretion increased on both HS diets compared to MK/LS (p < 0.05) and potassium excretion was increased on the HK diet compared to MK/LS and MK/HS (p < 0.05) confirming diet compliance. FMD was lower in MK/HS (5.4 ± 0.5%) compared to MK/LS (6.7 ± 0.5%; p < 0.05) and HK/HS (6.4 ± 0.5%), while there was no difference between the MK/LS and HK/HS diets (p > 0.05). These data suggest that dietary potassium provides vascular protection against the deleterious effects of high dietary sodium by restoring conduit artery function.
| S-EPMC7281996 | biostudies-literature
Project description:Hypertension is affected by both genetic and dietary factors. This study aimed to examine the interaction between dietary sodium/potassium intake, sodium-potassium ratios, and FGF5 rs16998073 and link these with increased risk for developing hypertension. Using data from the Health Examinee (HEXA) Study of the Korean Genome and Epidemiologic Study (KoGES), we were able to identify a total of 17,736 middle-aged Korean adults who could be included in our genome-wide association study (GWAS) to confirm any associations between hypertension and the FGF5 rs16998073 variant. GWAS analysis revealed that the FGF5 rs16698073 variant demonstrated the strongest association with hypertension in this population. Multivariable logistic regression was used to examine the relationship between dietary intake of sodium, potassium, and sodium-potassium ratios and the FGF5 rs16998073 genotypes (AA, AT, TT) and any increased risk of hypertension. Carriers with at least one minor T allele for FGF5 rs16998073 were shown to be at significantly higher risk for developing hypertension. Male TT carriers with a daily sodium intake ≥2000 mg also demonstrated an increased risk for developing hypertension compared to the male AA carriers with daily sodium intake <2000 mg (adjusted odds ratio (AOR) = 2.41, 95% confidence intervals (CIs) = 1.84-3.15, p-interaction < 0.0001). Female AA carriers with a daily potassium intake ≥3500 mg showed a reduced risk for hypertension when compared to female AA carriers with a daily potassium intake <3500 mg (AOR = 0.75. 95% CIs = 0.58-0.95, p-interaction < 0.0001). Male TT carriers in the mid-tertile for sodium-potassium ratio values showed the highest odds ratio for hypertension when compared to male AA carriers in the lowest-tertile for sodium-potassium ratio values (AOR = 3.03, 95% CIs = 2.14-4.29, p-interaction < 0.0001). This study confirmed that FGF5 rs16998073 variants do place their carriers (men and women) at increased risk for developing hypertension. In addition, we showed that high daily intake of sodium exerted a synergistic effect for hypertension when combined with FGF5 rs16998073 variants in both genders and that dietary sodium, potassium, and sodium-potassium ratios all interact with FGF5 rs16998073 and alter the risk of developing hypertension in carriers of either gender among Koreans.
| S-EPMC7400941 | biostudies-literature
Project description:The thiazide-sensitive sodium-chloride cotransporter (NCC) in the renal distal convoluted tubule (DCT) plays a critical role in regulating blood pressure (BP) and K+ homeostasis. During hyperkalemia, reduced NCC phosphorylation and total NCC abundance facilitate downstream electrogenic K+ secretion and BP reduction. However, the mechanism for the K+-dependent reduction in total NCC levels is unknown. Here, we show that NCC levels were reduced in ex vivo renal tubules incubated in a high-K+ medium for 24-48 h. This reduction was independent of NCC transcription, but was prevented using inhibitors of the proteasome (MG132) or lysosome (chloroquine). Ex vivo, high K+ increased NCC ubiquitylation, but inhibition of the ubiquitin conjugation pathway prevented the high K+-mediated reduction in NCC protein. In tubules incubated in high K+ media ex vivo or in the renal cortex of mice fed a high K+ diet for 4 days, the abundance and phosphorylation of heat shock protein 70 (Hsp70), a key regulator of ubiquitin-dependent protein degradation and protein folding, were decreased. Conversely, in similar samples the expression of PP1α, known to dephosphorylate Hsp70, was also increased. NCC coimmunoprecipitated with Hsp70 and PP1α, and inhibiting their actions prevented the high K+-mediated reduction in total NCC levels. In conclusion, we show that hyperkalemia drives NCC ubiquitylation and degradation via a PP1α-dependent process facilitated by Hsp70. This mechanism facilitates K+-dependent reductions in NCC to protect plasma K+ homeostasis and potentially reduces BP.
| S-EPMC8318901 | biostudies-literature
Project description:BackgroundDietary sodium may influence cognitive function through its effects on cerebrovascular function and cerebral blood flow.MethodsThe aim of this study was to evaluate the association of dietary sodium intake with cognitive decline in community-dwelling older adults. We also evaluated the associations of dietary potassium and sodium:potassium intake with cognitive decline, and associations of these nutrients with micro- and macro-structural brain magnetic resonance imaging (MRI) indices. In all, 1,194 participants in the Health Aging and Body Composition study with measurements of dietary sodium intake (food frequency questionnaire [FFQ]) and change in the modified Mini Mental State Exam (3MS) were included.ResultsThe age of participants was 74 ± 3 years with a mean dietary sodium intake of 2,677 ± 1,060 mg/day. During follow-up (6.9 ± 0.1 years), 340 (28%) had a clinically significant decline in 3MS score (≥1.5 SD of mean decline). After adjustment, dietary sodium intake was not associated with odds of cognitive decline (OR 0.96, 95% CI 0.50-1.84 per doubling of sodium). Similarly, potassium was not associated with cognitive decline; however, higher sodium:potassium intake was associated with increased odds of cognitive decline (OR 2.02 [95% CI 1.01-4.03] per unit increase). Neither sodium or potassium alone nor sodium:potassium were associated with micro- or macro-structural brain MRI indices. These results are limited by the use of FFQ.ConclusionsIn community-dwelling older adults, higher sodium:potassium, but not sodium or potassium intake alone, was associated with decline in cognitive function, with no associations observed with micro- and macro-structural brain MRI indices. These findings do not support reduction dietary sodium/increased potassium intake to prevent cognitive decline with aging.
| S-EPMC5815363 | biostudies-literature
Project description:IntroductionHypertension (HTN) is the leading cause of disease and death on a global scale. Diet's sodium and potassium levels may synergistically affect blood pressure. Currently, the sodium-to-potassium (Na/K) ratio is becoming a more reliable indicator. There has not been a systematic investigation of the dose-response relationship between dietary sodium, potassium, the Na/K ratio and the incidence of HTN based on the same study criteria. This study will conduct a thorough dose-response meta-analysis of cohort studies to estimate the effects of dietary sodium, potassium, and the Na/K ratio on the incidence of HTN to provide the most accurate reference for sodium and potassium intake.Methods and analysisWe will identify all relevant prospective and retrospective cohort studies by searching PubMed, Embase and Web of Science (from inception until December 2022). Exposures are 24 hours urinary excretions, and the outcome is the incidence of HTN. Two researchers will perform the literature selection and data extraction separately. The Newcastle-Ottawa Scale will be used to evaluate the quality of the included studies. We will use both linear and non-linear regression models to investigate the dose-response relationship among different levels (≥3) of sodium, potassium, Na/K ratio intake and the incidence of HTN (OR/RR/HR). Subgroup and sensitivity analyses will be applied to assess the potential heterogeneity sources and examine the stability of the results. We will also evaluate heterogeneity across studies and publication bias. Stata V.15.0 and RevMan V.5.0 will be used for statistical analyses.Ethics and disseminationAccording to the Institutional Review Board/Independent Ethics Committee of the Guang'anmen Hospital of the China Academy of Chinese Medical Science, this systematic meta-analysis protocol does not require ethical approval or informed consent. This meta-analysis will be published in a scientific journal with peer reviews.Prospero registration numberCRD42022331203.
| S-EPMC9923265 | biostudies-literature
Project description:Pentraxin-3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt-induced hypertension. We investigated the responses of pentraxin-3 to sodium and potassium supplementation to elucidate the potential role of pentraxin-3 in salt-induced hypertension. A total of 48 participants from northwest China were enrolled. All participants were maintained on a 3-day normal diet, which was sequentially followed by a 7-day low-sodium diet, a 7-day high-sodium diet, and a 7-day high-sodium plus potassium diet. Plasma concentrations of pentraxin-3 were assessed using ELISA. Plasma pentraxin-3 decreased significantly during the low-salt period compared to baseline (0.57 ± 0.19 ng/mL vs 0.72 ± 0.33 ng/mL, P = .012) and increased during the high-salt period (0.68 ± 0.26 ng/mL vs 0.57 ± 0.19 ng/mL, P = .037). Potassium supplementation inhibited salt-induced increase in pentraxin-3 (0.56 ± 0.21 ng/mL vs 0.68 ± 0.26 ng/mL, P = .015). Ln-transformed pentraxin-3 at baseline was inversely correlated with BMI (r = -.349, P = .02), DBP (r = -.414, P = .005), MAP (r = -.360, P = .017). We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-hour urinary sodium during low and high Na+ periods (r = .269, P = .012) and a negative relationship with 24 hours urinary potassium excretion during high-salt and high-salt plus potassium periods (r = -.246, P = .02). These correlations remained significant after adjusting for confounders. Pentraxin-3 responses were more prominent in salt-sensitive individuals than salt-resistant individuals. Dietary salt and potassium interventions significantly altered circulating pentraxin-3.
| S-EPMC8031200 | biostudies-literature