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Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

ABSTRACT: Acute dietary salt intake may cause an elevation in blood pressure (BP). The study aimed to assess the acute effect of saline loading on BP in subjects with different levels of salt intake. This study is based on the baseline survey of systemic epidemiology of salt sensitivity study. The sodium excretion in the 24-hour urine was calculated for estimating the level of salt intake. Subjects were performed an acute oral saline loading test (1 L), and data of 2019 participants were included for analyses. Multivariate linear regression and stratified analyses were performed to identify associations between 24-hour urinary sodium (24hUNa) with BP changes. Due to saline loading, systolic BP (SBP), pulse pressure, and urinary sodium concentration were significantly increased, while diastolic BP, heart rate, and urinary potassium concentration were significantly decreased. The SBP increments were more significant in subjects with lower salt intake, normotensives, elders, males, smokers, and drinkers. There was a significant linear negative dose-response association between SBP increment with 24hUNa (β = -0.901, 95% CI: -1.253, -0.548), especially in lower salt intake individuals (β = -1.297, 95% CI: -2.338, -0.205) and hypertensive patients (β = -1.502, 95% CI: -2.037, -0.967). After excluding patients who received antidiabetic or antihypertensive medicines, the effects of negative associations weakened but remained significantly. In conclusion, acute salt loading leads to an increment in SBP, and the increased SBP was negatively related with 24hUNa. This study indicated avoiding acute salt loading was important for escaping acute BP changes, especially in lower salt intake populations.

SUBMITTER: Peng W

PROVIDER: S-EPMC8029760 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

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Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

Peng Wenjuan W Xie Yunyi Y Liu Kuo K Qi Han H Liu Zheng Z Xia Juan J Cao Han H Guo Chunyue C Sun Yanyan Y Liu Xiaohui X Li Bingxiao B Wen Fuyuan F Zhang Fengxu F Zhang Ling L

Journal of clinical hypertension (Greenwich, Conn.) 20201121 2

Acute dietary salt intake may cause an elevation in blood pressure (BP). The study aimed to assess the acute effect of saline loading on BP in subjects with different levels of salt intake. This study is based on the baseline survey of systemic epidemiology of salt sensitivity study. The sodium excretion in the 24-hour urine was calculated for estimating the level of salt intake. Subjects were performed an acute oral saline loading test (1 L), and data of 2019 participants were included for anal ...[more]

PMID: 33220161

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Project description:Excessive salt intake is one of the causes of hypertension, and reducing salt intake is important for managing the risk of hypertension and subsequent cardiovascular events. Esaxerenone, a mineralocorticoid receptor blocker, has the potential to exert an antihypertensive effect in hypertensive patients with excessive salt intake, but evidence is still lacking, especially in clinical settings. We aimed to determine if baseline sodium/potassium ratio and baseline estimated 24-h urinary sodium excretion can predict the antihypertensive effect of esaxerenone in patients with essential hypertension inadequately controlled with an angiotensin receptor blocker (ARB) or a calcium channel blocker (CCB). This was an exploratory, open-label, interventional study with a 4-week observation period and a 12-week treatment period. Esaxerenone was orally administered once daily in accordance with the Japanese package insert. In total, 126 patients met the eligibility criteria and were enrolled (ARB subcohort, 67; CCB subcohort, 59); all were included in the full analysis set (FAS) and safety analysis. In the FAS, morning home systolic blood pressure (SBP)/diastolic blood pressure (DBP) significantly decreased from baseline to end of treatment (primary efficacy endpoint) (-11.9 ± 10.9/ - 6.4 ± 6.8 mmHg, both p < 0.001); a similar trend was observed in both subcohorts. Significant reductions were also shown in bedtime home and office SBP/DBP (all p < 0.001). Each BP change was consistent regardless of the urinary sodium/potassium ratio or estimated 24-h urinary sodium excretion at baseline. The urinary albumin-creatinine ratio (UACR) and N-terminal pro-brain natriuretic peptide (NT-proBNP) significantly decreased from baseline to Week 12 in the total population and both subcohorts. No new safety concerns were raised. Esaxerenone significantly decreased morning home, bedtime home, and office BP; UACR; and NT-proBNP in this patient population, regardless of concomitant ARB or CCB use. The antihypertensive effect of esaxerenone was independent of the urinary sodium/potassium ratio and estimated 24-h urinary sodium excretion at baseline.

Project description:Background: PAHO-WHO reports that sodium intake is currently high in the Caribbean. The objective was to estimate sodium (Na) and potassium (K) intakes by 72 h dietary recall and compare them with those obtained from 24 h urinary excretion in Dominican adults. Methods: A total of 69 adults (33 men) completed a 3-day dietary recall with emphasis on added salt and seasonings. The 24 h urine samples were analysed by indirect potentiometry using the membrane ion-selective electrode technique. The WHO-PAHO Questionnaire on Knowledge, Attitudes and Behaviour toward Dietary Salt and Health was completed. Results: Dietary Na intake ranged from 1.0 to 8.3 g. Median dietary and urinary Na concentrations were similar (2.7 and 2.5 mmol/d). Mean dietary Na and K concretertentrations were higher than those excreted in 24 h urine (133.0 ± 59.7 vs. 103.7 ± 44.5 mmol Na/d, p = 0.001; 69.0 ± 21.0 vs. 36 ± 16.3 mmol K/d, p < 0.001). The Na-to-K ratio was lower in dietary than in 24 h urine samples (2.0 ± 1.1 vs. 3.2 ± 1.6 mmol/d, p < 0.001). Urinary Na concentration was associated with sex (r = 0.280, p = 0.020) and obesity (r = 0.244, p = 0.043) and K with sex (r = 0.356, p = 0.003). Urinary Na-to-K was inversely related to age (r= -0.291, p = 0.015). Sex and obesity explained 11% of the variance in urinary Na concentration and sex only of the variance in urinary K concentration. The only significant correlation between dietary and urinary concentrations was that of K (r = 0.342, p = 0.004). This correlation matrix, controlled for overweight and sex, maintained the level of significance and was equal in almost 12% of the data. Conclusions: These data, which are the first data on Na and K intakes in Dominicans assessed by dietary assessment, showed a higher mean sodium intake (mean of dietary recall and urinary excretion data: 2.7 g Na, 6.8 g salt/day) and a lower K intake (2.06 g/day) than the WHO recommendations (<2.0 g Na, ≥3.5 g K). Potassium, but not sodium, intake from 72 h food recall and 24 h urinary excretion showed a correlation when controlling for sex and obesity, but not enough to consider them interchangeable.

Dataset Information

Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

Publications

Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

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