Key result
Low-sodium diet cuts urinary marinobufagenin ~17% alongside reductions in systolic BP and aortic stiffness.
Why the study?
Systolic BP and large elastic artery stiffness increase with age and are reduced by dietary sodium restriction, but the role of marinobufagenin in this process is unclear.
Does dietary sodium restriction reduce urinary marinobufagenin excretion, systolic BP, and aortic stiffness in middle-aged/older adults with moderately elevated systolic BP?
RCT (n=11)
placebo-controlled
randomized crossover
Does dietary sodium restriction reduce urinary marinobufagenin excretion, systolic BP, and aortic stiffness in middle-aged/older adults with moderately elevated systolic BP?
Absolute Event Rate: 25.4% vs 30.7%
p-value: p=<0.05
Dietary sodium restriction reduces urinary marinobufagenin excretion, which is positively associated with systolic blood pressure and aortic stiffness in humans.
Supports low-sodium diet to lower BP and aortic stiffness in elevated-BP adults; extends evidence for marinobufagenin reduction as a modifiable link.
BACKGROUND AND OBJECTIVES: Systolic BP and large elastic artery stiffness both increase with age and are reduced by dietary sodium restriction. Production of the natriuretic hormone marinobufagenin, an endogenous α1 Na+,K+-ATPase inhibitor, is increased in salt-sensitive hypertension and contributes to the rise in systolic BP during sodium loading. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: The hypothesis was that dietary sodium restriction performed in middle-aged/older adults (eight men and three women; 60 ± 2 years) with moderately elevated systolic BP (139 ± 2/83 ± 2 mmHg) would reduce urinary marinobufagenin excretion as well as systolic BP and aortic pulse-wave velocity (randomized, placebo-controlled, and crossover design). This study also explored the associations among marinobufagenin excretion with systolic BP and aortic pulse-wave velocity across conditions of 5 weeks of a low-sodium (77 ± 9 mmol/d) and 5 weeks of a normal-sodium (144 ± 7 mmol/d) diet. RESULTS: Urinary marinobufagenin excretion (weekly measurements; 25.4 ± 1.8 versus 30.7 ± 2.1 pmol/kg per day), systolic BP (127 ± 3 versus 138 ± 5 mmHg), and aortic pulse-wave velocity (700 ± 40 versus 843 ± 36 cm/s) were lower during the low- versus normal-sodium condition (all P<0.05). Across all weeks, marinobufagenin excretion was related with systolic BP (slope=0.61, P<0.001) and sodium excretion (slope=0.46, P<0.001). These associations persisted during the normal- but not the low-sodium condition (both P<0.005). Marinobufagenin excretion also was associated with aortic pulse-wave velocity (slope=0.70, P=0.02) and endothelial cell expression of NAD(P)H oxidase-p47phox (slope=0.64, P=0.006). CONCLUSIONS: These results show, for the first time in humans, that dietary sodium restriction reduces urinary marinobufagenin excretion and that urinary marinobufagenin excretion is positively associated with systolic BP, aortic stiffness (aortic pulse-wave velocity), and endothelial cell expression of the oxidant enzyme NAD(P)H oxidase. Importantly, marinobufagenin excretion is positively related to systolic BP over ranges of sodium intake typical of an American diet, extending previous observations in rodents and humans fed experimentally high-sodium diets.
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Jablonski et al. (2013) conducted an RCT in moderately elevated systolic BP (n=11). Low-sodium diet vs. Normal-sodium diet (144 ± 7 mmol/d) was evaluated on Urinary marinobufagenin excretion (pmol/kg per day) (p=<0.05). A 5-week low-sodium diet reduced urinary marinobufagenin excretion (25.4 vs 30.7 pmol/kg per day, P<0.05), systolic BP, and aortic stiffness compared to a normal-sodium diet.
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