Blood pressure is reduced by short-time calorie restriction in overweight hypertensive women with a constant intake of sodium and potassium

1993 ◽  
Vol 11 (5) ◽  
pp. S320???S321 ◽  
Author(s):  
Minoru Kawamura ◽  
Takayuki Akasaka ◽  
Tamako Kasatsuki ◽  
Jun Nakajima ◽  
Seiki Onodera ◽  
...  
Hypertension ◽  
1996 ◽  
Vol 27 (3) ◽  
pp. 408-413 ◽  
Author(s):  
Minoru Kawamura ◽  
Toshiyuki Adachi ◽  
Jun Nakajima ◽  
Takuya Fujiwara ◽  
Katsuhiko Hiramori

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Lieke Gijsbers ◽  
James Dower ◽  
Marco Mensink ◽  
Johanna M Geleijnse

Introduction: We performed a 12-week randomized placebo-controlled crossover study to examine the effects of sodium and potassium supplementation on blood pressure (BP) and arterial stiffness in untreated (pre)hypertensive individuals on a low-sodium, low-potassium diet. Methods: During the study, subjects were on a fully controlled diet that provided on average 2.4 g/d of sodium (equals 6 g/d of salt) and 2.2 g/d of potassium. After a 1-week run-in period, 37 subjects received capsules with supplemental sodium (3 g/d, equals 7.5 g/d of salt), supplemental potassium (3 g/d), or placebo, for four weeks each (not separated by wash-out), in random order. Fasting office BP, 24-h ambulatory BP, and measures of arterial stiffness (SphygmoCor®) were assessed at baseline and after each treatment. Results: Subjects had a mean pre-treatment BP of 145/81 mmHg and 68% (25 of 37) had systolic BP (SBP) ≥140 mmHg. In 36 subjects who completed the study, sodium supplementation increased urinary sodium by 97.6 mmol/24h (2.2 g/d) and potassium supplementation increased urinary potassium by 62.9 mmol/24h (2.5 g/d), compared to placebo (Table). Sodium supplementation significantly increased office BP by 7.5/3.3 mmHg, 24-h BP by 7.0/2.1 mmHg and central BP by 8.5/3.6 mmHg. Potassium supplementation significantly reduced 24-h BP by 4.0/1.7 mmHg. Measures of arterial stiffness did not change. Conclusion: Increasing the intake of sodium has a strong adverse effect on BP in untreated (pre)hypertensive individuals. Increased potassium intake, however, lowers BP even when people are on a reduced sodium diet. Short-term changes in sodium and potassium intake have little effect on arterial stiffness. Trial registration: ClinicalTrials.gov Identifier: NCT01575041


1980 ◽  
Vol 59 (s6) ◽  
pp. 161s-164s ◽  
Author(s):  
P. S. Parfrey ◽  
P. Wright ◽  
J. M. Ledingham

1. The diurnal excretion of sodium and potassium was observed in young people, with and without a genetic predisposition to hypertension, both in the presence and absence of psychological stress. 2. In the absence of stress, the normal day/night sodium excretion ratio was reversed in the children of hypertensive parents. This was significantly less than day/night sodium excretion in children of normotensive parents. A similar finding was observed for day/night potassium excretion. 3. There was a significant negative correlation between systolic blood pressure and day/night sodium excretion in children of hypertensive parents but not in children of normotensive parents. 4. After the mental stress of a University examination day/night sodium reverted to normal in children of hypertensive parents.


Hypertension ◽  
1994 ◽  
Vol 23 (6_pt_1) ◽  
pp. 729-736 ◽  
Author(s):  
A R Dyer ◽  
P Elliott ◽  
M Shipley ◽  
R Stamler ◽  
J Stamler

1998 ◽  
Vol 76 (1) ◽  
pp. 63-67 ◽  
Author(s):  
María Reverte ◽  
Olga Flores ◽  
Belén Gallego ◽  
Antonio Lestón ◽  
José Miguel López-Novoa

We have studied during 30 days the effect of a low dose of NG-nitro-L-arginine methyl ester (1 mg ·kg-1 ·day-1 in drinking water) in the presence of D- or L-arginine (1 mg ·kg-1 ·day-1 in drinking water) in comparison with D- or L-arginine alone on blood pressure and renal function in conscious uninephrectomized female spontaneously hypertensive rats. At the end of the study, there was a significant increase in systolic blood pressure in the NG-nitro-L-arginine methyl ester + D-arginine group (307 ± 6 mmHg (1 mmHg = 133.3 Pa), n = 14, p << 0.05) in comparison with NG-nitro-L-arginine methyl ester + L-arginine (281 ± 6 mmHg, n = 14), L-arginine (262 ± 5 mmHg, n = 13), and D-arginine (258 ± 7 mmHg, n = 12) groups. There were no changes in diuresis, proteinuria, or sodium and potassium excretion between differently treated animals during this study. These results suggest that in uninephrectomized female spontaneously hypertensive rats, after 1 month blockade of NO synthesis with a low dose of NG-nitro-L-arginine methyl ester, vasculature is under tonic control by NO and it is not correlated with renal dysfunction.Key words: Key words: NG -nitro-L-arginine methyl ester (L-NAME), kidney, hypertension, spontaneously hypertensive rats, renaldysfunction, uninephrectomy.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Zefeng Zhang ◽  
Mary Cogswell ◽  
Cathleen Gillespie ◽  
Jing Fang ◽  
Shifan Dai ◽  
...  

Introduction: Evidence from randomized controlled trials demonstrates higher sodium and/or lower potassium intake increase blood pressure and the risk of hypertension. However, the relationship between sodium, potassium and blood pressure has not been examined using nationally representative sample and estimated usual intakes of these nutrients. Hypothesis: We hypothesized that usual sodium and potassium intake have opposing effects on blood pressure and a higher sodium-to-potassium ratio is associated with elevated blood pressure and hypertension. Methods: We analyzed data on 12,854 participants aged 20 years and older from the 2003-2008 National Health and Nutrition Examination Surveys. We estimated the usual intakes of sodium and potassium from the diet accounting for measurement error. Mean blood pressure was calculated from up to three readings on each subject and hypertension included both diagnosed and undiagnosed hypertension. We used multivariable linear regression to examine the associations between intakes of sodium, potassium and their ratio with systolic and diastolic blood pressure, and logistic regression for associations with hypertension. Results: The average estimated usual intakes of sodium and potassium were 3465 and 2741 mg/d, respectively. The average sodium-to-potassium ratio was 1.39; higher ratios were observed among males, younger and non-Hispanic black participants. After adjustment for potential confounders, usual intakes of sodium, potassium and their ratio were significantly associated with systolic blood pressure, with an increase of 1.08 mm Hg (95% confidence interval (CI): 0.30 – 1.86) and a decrease of 1.47 mmHg (95% CI: -2.31, -0.63) for every 1000 mg/d increase in sodium and potassium intake, respectively, and an increase of 2.80 mmHg (95% CI: 0.90 - 4.70) for every unit increase in sodium-to-potassium ratio. No association was found for diastolic blood pressure. The adjusted odds ratio (OR) comparing the highest and lowest quartiles of usual sodium or potassium intakes were 1.63 (95% CI: 1.14 - 2.34) and 0.61 (95% CI: 0.45 - 0.82), respectively, for risk of hypertension. For sodium-to-potassium ratio, the adjusted OR was 1.49 (95% CI: 1.17 - 1.89). The patterns of association were largely consistent across age, gender, race/ethnicity, body mass index, and education subgroups. Conclusions: In conclusion, our results indicated higher sodium and lower potassium intakes were associated with increased systolic blood pressure and risk for hypertension. The combined effect of sodium and potassium might play a central role in the pathogenesis of hypertension. The results further confirm that reducing sodium and increasing potassium intakes concurrently may have important implications in the prevention of hypertension, and hence, of cardiovascular disease.


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