scholarly journals Hyperosmolarity and Increased Serum Sodium Concentration Are Risks for Developing Hypertension Regardless of Salt Intake: A Five-Year Cohort Study in Japan

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1422
Author(s):  
Masanari Kuwabara ◽  
Mehmet Kanbay ◽  
Koichiro Niwa ◽  
Ryusuke Ae ◽  
Ana Andres-Hernando ◽  
...  

The potential contribution of serum osmolarity in the modulation of blood pressure has not been evaluated. This study was done to examine the relationship between hyperosmolarity and hypertension in a five-year longitudinal design. We enrolled 10,157 normotensive subjects without diabetes who developed hypertension subsequently as determined by annual medical examination in St. Luke’s International Hospital, Tokyo, between 2004 and 2009. High salt intake was defined as >12 g/day by a self-answered questionnaire and hyperosmolarity was defined as >293 mOsm/L serum osmolarity, calculated using serum sodium, fasting blood glucose, and blood urea nitrogen. Statistical analyses included adjustments for age, gender, body mass index, smoking, drinking alcohol, dyslipidemia, hyperuricemia, and chronic kidney disease. In the patients with normal osmolarity, the group with high salt intake had a higher cumulative incidence of hypertension than the group with normal salt intake (8.4% versus 6.7%, p = 0.023). In contrast, in the patients with high osmolarity, the cumulative incidence of hypertension was similar in the group with high salt intake and in the group with normal salt intake (13.1% versus 12.9%, p = 0.84). The patients with hyperosmolarity had a higher incidence of hypertension over five years compared to that of the normal osmolarity group (p < 0.001). After multiple adjustments, elevated osmolarity was an independent risk for developing hypertension (OR (odds ratio), 1.025; 95% CI (confidence interval), 1.006–1.044), regardless of the amount of salt intake. When analyzed in relation to each element of calculated osmolarity, serum sodium and fasting blood glucose were independent risks for developing hypertension. Our results suggest that hyperosmolarity is a risk for developing hypertension regardless of salt intake.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Loren Safta ◽  
Shiri Levy-Basso ◽  
Joseph Levy

Abstract Diabetic kidney hypertrophy may contribute to the development of diabetic kidney disease. Hyperglycemia is recognized as a cause for the kidney endangerment. Salt may accelerate progression of kidney disease in diabetes. To further study the effect of high salt intake on kidney disease we used neonatal streptozotocin induced Noninsulin Dependent Diabetic (NIDD) rats fed ad libitum with regular Purina chow and 2% salt Purina chow. Rats in 5 groups were sacrificed at 6 weeks. Each group had 5–7 rats of diabetics on 2% salt and on regular chow and controls on 2% salt and on regular chow. Blood glucose in diabetics on salt ranged between 185±19–576±20 and in diabetics on regular chow 184±20–458±78 mg/dl. Controls on 2% salt 105±8.6–133±10.3 and controls on regular chow 110±8.9 - 130±3.11. Kidney weights in diabetics on salt was 1.85±0.09–2.0±0.06 gr, diabetics on regular chow 1.6±0.04 - 1.56±0.06 controls on salt 1.19±0.03–1.32±0.05 and controls on regular chow 1.23±0.03. Blood glucose in diabetics on salt and on regular chow was higher than in controls p˂0.05 but did not differ between the diabetic groups. Kidney weight was increased in both diabetic groups compared with controls p˂0.05 and was increased in diabetics on salt compared with diabetics on regular chow p˂0.05 at all glucose levels. Controls on salt and on regular chow had similar kidney weights. Also kidney weight relative to body weight was higher in diabetics than in controls p˂0.05 and was higher in diabetics on salt compared to diabetics on regular chow p˂0.05, but there was no difference between controls on salt and controls on regular diet. Kidney % of water was similar in all four groups but protein to kidney DNA ratio was higher in the diabetic groups p˂0.05 confirming the kidney hypertrophy. Insulin sensitivity measured in controls was not different between groups when glucose transport, glucose oxidation and lipogenesis were measured in fat cells showing no effect of salt on insulin sensitivity. We suggest that high salt intake is an additional risk factor for increased kidney weight in NIDDM that is additive to that of the prevailing glycemia.


2020 ◽  
Author(s):  
Sepiso Kenias Masenga ◽  
Leta Pilic ◽  
Benson M. Hamooya ◽  
Selestine Nzala ◽  
Geoffrey Kwenda ◽  
...  

Abstract ObjectiveHypertension and dietary salt are associated with inflammation in murine models. Studies in humans are scare and yet critical for the prevention and treatment of hypertension. This was an interventional study of 85 participants. Participants were instructed to follow a one week of low (4 g/day)- and high (9 g/day)-salt diet. BioLegend’s LEGENDplex™ bead-based immunoassay (USA) was used to quantify cytokine levels in plasma. Mann-Whitney, logistic regression and the Wilcoxon matched-pairs signed-rank test were used to compare inflammation markers on low- and high-salt diets. The goal of this study was to determine the association between hypertension and inflammation and the effect of high dietary salt intake on pro- and anti-inflammatory cytokines in HIV positive and HIV negative individuals.Results43 participants among the 85 were hypertensive with equal sex distribution. Hypertensives had higher plasma levels of IL-6, IL-17A, tumor necrosis factor-alpha, monocyte count and fasting blood glucose. High salt intake was associated with higher IL-2 in hypertensive persons with HIV and lower IL-21 plasma levels in the HIV-negative. These findings suggest that there is an association between hypertension, salt and inflammation. Hypertension is associated with inflammation, and dietary salt intake may play a role in modulating inflammation.RegistrationPan African Clinical Trial Registry (www.pactr.org) PACTR202007493610166. Retrospectively registered.


2012 ◽  
Vol 18 (8) ◽  
pp. 691-701 ◽  
Author(s):  
Xiu-Yang Li ◽  
Xian-Lei Cai ◽  
Ping-Da Bian ◽  
Liu-Ru Hu

2011 ◽  
Vol 209 (1) ◽  
pp. 85-94 ◽  
Author(s):  
Karine Bibeau ◽  
Mélissa Otis ◽  
Jean St-Louis ◽  
Nicole Gallo-Payet ◽  
Michèle Brochu

In low sodium-induced intrauterine growth restricted (IUGR) rat, foetal adrenal steroidogenesis as well as the adult renin–angiotensin–aldosterone system (RAAS) is altered. The aim of the present study was to determine the expression of cytochrome P450 aldosterone synthase (P450aldo) and of angiotensin II receptor subtypes 1 (AT1R) and 2 (AT2R) in adult adrenal glands and whether this expression could be influenced by IUGR and by high-salt intake in a sex-specific manner. After 6 weeks of 0.9% NaCl supplementation, plasma renin activity, P450aldo expression and serum aldosterone levels were decreased in all groups. In males, IUGR induced an increase in AT1R, AT2R, and P450aldo levels, without changes in morphological appearance of the zona glomerulosa (ZG). By contrast, in females, IUGR had no effect on the expression of AT1R, but increased AT2R mRNA while decreasing protein expression of AT2R and P450aldo. In males, salt intake in IUGR rats reduced both AT1R mRNA and protein, while for AT2R, mRNA levels decreased whereas protein expression increased. In females, salt intake reduced ZG size in IUGR but had no affect on AT1R or AT2R expression in either group. These results indicate that, in response to IUGR and subsequently to salt intake, P450aldo, AT1R, and AT2R levels are differentially expressed in males and females. However, despite these adrenal changes, adult IUGR rats display adequate physiological and adrenal responses to high-salt intake, via RAAS inhibition, thus suggesting that extra-adrenal factors likely compensate for ZG alterations induced by IUGR.


2014 ◽  
Vol 2 (8) ◽  
pp. e12110 ◽  
Author(s):  
Clare M. Reynolds ◽  
Mark H. Vickers ◽  
Claudia J. Harrison ◽  
Stephanie A. Segovia ◽  
Clint Gray

1984 ◽  
Vol 6 ◽  
pp. S95 ◽  
Author(s):  
L. H. Block ◽  
B. E. Lütold ◽  
P. Bolli ◽  
W. Kiowski ◽  
F. R. Bühler

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