scholarly journals Dietary Sodium Restriction Reverses Vascular Endothelial Dysfunction in Middle-Aged/Older Adults With Moderately Elevated Systolic Blood Pressure

2013 ◽  
Vol 61 (3) ◽  
pp. 335-343 ◽  
Author(s):  
Kristen L. Jablonski ◽  
Matthew L. Racine ◽  
Candace J. Geolfos ◽  
Phillip E. Gates ◽  
Michel Chonchol ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Older Adults ◽  
Endothelial Dysfunction ◽  
Systolic Blood Pressure ◽  
Dietary Sodium ◽  
Vascular Endothelial ◽  
Sodium Restriction ◽  
Vascular Endothelial Dysfunction ◽  
Middle Aged ◽  
Elevated Systolic Blood Pressure

scholarly journals Dietary sodium restriction decreases urinary NGAL in older adults with moderately elevated systolic blood pressure free from chronic kidney disease

2020 ◽  
Vol 68 (7) ◽  
pp. 1271-1275
Author(s):  
Wei Wang ◽  
Michel Chonchol ◽  
Douglas R Seals ◽  
Kristen L Nowak
Keyword(s):  
Blood Pressure ◽  
Older Adults ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Systolic Blood Pressure ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Tubular Injury ◽  
Urinary Creatinine ◽  
Elevated Systolic Blood Pressure

Increased aortic stiffness may contribute to kidney damage by transferring excessive flow pulsatility to susceptible renal microvasculature, leading to constriction or vessel loss. We previously demonstrated that 5 weeks of dietary sodium restriction (DSR) reduces large-elastic artery stiffness as well as blood pressure in healthy middle-aged/older adults with moderately elevated systolic blood pressure (SBP) who are free from chronic kidney disease (CKD). We hypothesized that DSR in this cohort would also reduce urinary concentrations of renal tubular injury biomarkers, which predict incident CKD in the general population. We performed a post hoc analysis using stored 24 hours urine samples collected in 13 participants as part of a randomized, double-blind, crossover clinical trial of DSR (low sodium (LS) target: 50 mmol/day; normal sodium (NS) target: 150 mmol/day). Participants were 61±2 (mean±SEM) years (8 M/5 F) with a baseline blood pressure of 139±2/82±2 mm Hg and an estimated glomerular filtration rate of 79±3 mL/min/1.73 m2. Twenty-four hour urinary sodium excretion was reduced from 149±7 to 66±8 mmol/day during week 5. Despite having preserved kidney function, participants had a 31% reduction in urinary neutrophil gelatinase-associated lipocalin concentrations with just 5 weeks of DSR (LS: 2.8±0.6 vs NS: 4.2±0.8 ng/mL, p<0.05). Results were similar when normalized to urinary creatinine (urinary creatinine did not change between conditions). Concentrations of another kidney tubular injury biomarker, kidney injury molecule-1, were below the detectable limit in all but one sample. In conclusion, DSR reduces an established clinical biomarker of kidney tubular damage in adults with moderately elevated SBP who are free from prevalent kidney disease.

Sodium intake and the effects of isoproterenol and exercise on plasma renin in man

1978 ◽  
Vol 45 (6) ◽  
pp. 870-874 ◽  
Author(s):  
F. H. Leenen ◽  
P. Boer ◽  
G. G. Geyskes
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dynamic Exercise ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Dietary Sodium Restriction

Changes in heart rate, blood pressure, and plasma renin activity (PRA) were assessed during infusion of increasing doses of isoproterenol and during increasing work loads of dynamic exercise in five normal young men. Studies were performed at three levels of dietary sodium restriction: normal, moderately, and more severely restricted. Isoproterenol induced the expected dose-related increases in heart rate, systolic blood pressure, and PRA and decreases in diastolic blood pressure. Changes in dietary sodium intake affected these changes only to a minor degree. Dynamic exercise also induced the expected work-load-related increases in heart rate, systolic blood pressure, and PRA and decreases in diastolic blood pressure. Also these changes were not significantly affected by changes in dietary sodium intake. Apparently dietary sodium restriction does not sensitize the renin-releasing mechanisms to sympathetic stimulation.

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