Long-Term Adherence to Low-Sodium Diet in Patients With Heart Failure

2017 ◽  
Vol 39 (4) ◽  
pp. 553-567 ◽  
Author(s):  
Misook L. Chung ◽  
Linda Park ◽  
Susan K. Frazier ◽  
Terry A. Lennie

Although following a low-sodium diet (LSD) for heart failure (HF) has been recommended for decades, little is known about factors related to long-term patient adherence. The purposes of this study were to (a) compare sodium intake and factors affecting adherence in a long-term adherent group and in a non-adherent group and (b) examine predictors of membership in the long-term adherent group. Patients with HF ( N = 74) collected 24-hr urine samples and completed the Dietary Sodium Restriction Questionnaire and the Patient Health Questionnaire-9. Long-term adherence was determined using the Stage of Dietary Behavior Change Scale. The long-term adherent group had lower sodium intake (3,086 mg vs. 4,135 mg, p = .01) and perceived more benefits from LSD than the non-adherent group. Only positive attitudes toward LSD predicted membership in the long-term adherence group (odds ratio [OR] = 1.18, p = .005). Interventions focused on enhancing positive perceptions of the benefits of an LSD may improve long-term dietary adherence in patients with HF.

1989 ◽  
Vol 256 (6) ◽  
pp. E863-E871 ◽  
Author(s):  
H. Hisa ◽  
Y. H. Chen ◽  
K. J. Radke ◽  
J. L. Izzo ◽  
C. D. Sladek ◽  
...  

These experiments evaluated the contribution of alpha- and beta-adrenergic stimulation to plasma renin activity (PRA) during early and long-term dietary sodium restriction, compared with normal sodium intake. Uninephrectomized conscious dogs with catheters in the aorta, vena cava, and remaining renal artery were studied during normal sodium diet (approximately 70 meq/day), after 2-3 days of low-sodium diet (5-7 meq/day), and after greater than or equal to 2 wk of low-sodium diet. Direct renal arterial (ira) infusion of phenoxybenzamine plus propranolol decreased PRA by similar proportions (39-48%) during all three states of dietary sodium intake. The PRA achieved after adrenergic blockade remained higher (P less than 0.05) during early and long-term sodium restriction than during normal sodium intake. The effect on PRA of ira infusion of propranolol alone was not different from that of phenoxybenzamine plus propranolol during normal or low-sodium diet, and the magnitude of decrease in PRA during low-sodium diet was the same whether propranolol (1 microgram.kg-1.min-1) was infused ira or intravenously. In summary, beta-adrenergic stimulation accounts for similar proportions of PRA during early and long-term dietary sodium restriction and during normal sodium intake. Renal alpha-adrenoceptors appear to play little or no role in control of PRA under these conditions.


2020 ◽  
Vol 73 (4) ◽  
Author(s):  
Mailson Marques de Sousa ◽  
Bernadete de Lourdes André Gouveia ◽  
Taciana da Costa Farias Almeida ◽  
Maria Eliane Moreira Freire ◽  
Francisco de Assis Brito Pereira de Melo ◽  
...  

ABSTRACT Objectives: to analyze the scientific production about sodium restriction in patients with heart failure. Methods: integrative literature review from articles published from 2007 to 2017, located in the CINAHL and Scopus databases. Results: thirteen studies were analyzed. Sodium intake restriction was associated with lower unfavorable clinical outcomes in patients with marked symptomatology. The 24-hour urine sodium dosage was the main tool to assess adherence to the low sodium diet. Conclusions: based on the studies included in this review, in symptomatic patients, dietary sodium restriction should be encouraged in clinical practice as a protective measure for health. However, in asymptomatic patients, it should be well studied.


2013 ◽  
Vol 304 (3) ◽  
pp. R260-R266 ◽  
Author(s):  
Julie O'Neill ◽  
Alan Corbett ◽  
Edward J. Johns

Angiotensin II at the kidney regulates renal hemodynamic and excretory function, but the actions of an alternative metabolite, angiotensin (1–7), are less clear. This study investigated how manipulation of dietary sodium intake influenced the renal hemodynamic and excretory responses to intrarenal administration of angiotensin (1–7). Renal interstitial infusion of angiotensin (1–7) in anesthetized rats fed a normal salt intake had minimal effects on glomerular filtration rate but caused dose-related increases in urine flow and absolute and fractional sodium excretions ranging from 150 to 200%. In rats maintained for 2 wk on a low-sodium diet angiotensin (1–7) increased glomerular filtration rate by some 45%, but the diuretic and natriuretic responses were enhanced compared with those in rats on a normal sodium intake. By contrast, renal interstitial infusion of angiotensin (1–7) in rats maintained on a high-sodium intake had no effect on glomerular filtration rate, whereas the diuresis and natriuresis was markedly attenuated compared with those in rats fed either a normal or low-sodium diet. Plasma renin and angiotensin (1–7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. These findings demonstrate that the renal hemodynamic and excretory responses to locally administered angiotensin (1–7) is dependent on the level of sodium intake and indirectly on the degree of activation of the renin-angiotensin system. The exact way in which angiotensin (1–7) exerts its effects may be dependent on the prevailing levels of angiotensin II and its receptor expression.


2021 ◽  
Author(s):  
Rosa D Wouda ◽  
Femke Waanders ◽  
Dick de Zeeuw ◽  
Gerjan Navis ◽  
Liffert Vogt ◽  
...  

Abstract Background Angiotensin receptor blockers (ARBs) lower blood pressure (BP) and proteinuria and reduce renal disease progression in many—but not all—patients. Reduction of dietary sodium intake improves these effects of ARBs. Dietary potassium intake affects BP and proteinuria. We set out to address the effect of potassium intake on BP and proteinuria response to losartan in non-diabetic proteinuric chronic kidney disease (CKD) patients. Methods We performed a post-hoc analysis of a placebo-controlled interventional cross-over study in 33 non-diabetic proteinuric patients (baseline mean arterial pressure and proteinuria: 105 mmHg and 3.8 g/d, respectively). Patients were treated for 6 weeks with placebo, losartan, and losartan/hydrochlorothiazide, combined with a habitual (∼200 mmol/d) and low-sodium diet (<100 mmol/d), in randomized order. To analyze the effects of potassium intake, we categorized patients based on median split of 24 h urinary potassium excretion, reflecting potassium intake. Results Mean potassium intake was stable during all 6 treatment periods. Losartan and losartan/hydrochlorothiazide lowered BP and proteinuria in all treatment groups. Patients with high potassium intake showed no difference in the BP effects compared to patients with low potassium intake. The antiproteinuric response to losartan monotherapy and losartan combined with hydrochlorothiazide during the habitual sodium diet was significantly diminished in patients with high potassium intake (20% vs. 41%, p = 0.011 and 48% vs 64%, p = 0.036). These differences in antiproteinuric response abolished when shifting to the low sodium diet. Conclusions In proteinuric CKD patients, the proteinuria, but not BP-lowering response to losartan during a habitual high sodium diet was hampered during high potassium intake. Differences disappeared after sodium status change by low-sodium diet.


2018 ◽  
Vol 315 (4) ◽  
pp. E671-E675 ◽  
Author(s):  
Suman Srinivasa ◽  
Anna Aulinas ◽  
Timothy O’Malley ◽  
Patrick Maehler ◽  
Gail K. Adler ◽  
...  

Oxytocin, while classically known for its role in parturition, lactation, and social behavior, also has been implicated in the control of sodium homeostasis in animal models. To improve our understanding of oxytocin physiology in humans, we measured basal oxytocin levels under low- and liberal-dietary-sodium conditions and following a peripheral angiotensin II (ANG II) infusion. Ten healthy individuals underwent a 6-day standardized low-sodium diet and a 6-day liberal-sodium diet. Each diet was followed by a graded ANG II infusion for 30-min sequential intervals at doses of 0.3, 1.0, and 3.0 ng·kg−1·min−1. Fasting serum oxytocin was assessed before and after ANG II infusion. Basal oxytocin levels (1,498.5 ± 94.7 vs. 1,663.3 ± 213.9 pg/ml, P = 0.51) did not differ after the low- and liberal-sodium diets. Following the ANG II infusion, ANG II levels and mean arterial pressure significantly increased as expected. In contrast, the ANG II infusion significantly lowered oxytocin levels from 1,498.5 ± 94.7 vs. 1,151.7 ± 118.1 pg/ml ( P < 0.001) on the low-sodium diet and from 1,663.3 ± 213.9 vs. 1,095.2 ± 87.4 pg/ml ( P = 0.03) on the liberal-sodium diet. The percent change in oxytocin following the ANG II infusion did not differ by sodium diet (−25 ± 5% vs. −28 ± 7% low- vs. liberal-sodium conditions, P > 0.99). Dietary sodium intake did not affect circulating oxytocin levels among healthy individuals. Systemic oxytocin levels were significantly suppressed following a peripheral ANG II infusion independent of dietary sodium conditions.


1990 ◽  
Vol 258 (1) ◽  
pp. R187-R192 ◽  
Author(s):  
R. R. Vollmer ◽  
S. P. Corey ◽  
S. A. Meyers ◽  
E. M. Stricker ◽  
S. J. Fluharty

In confirmation of previous studies, the amount of epinephrine released into blood during electrical stimulation of the thoracolumbar region of the spinal cord in pithed rats on a low-sodium diet (0.01% sodium by weight of diet for 1 mo) was significantly greater than that observed in rats on a normal sodium diet (0.3% sodium by weight of diet). The present work assessed the extent to which endogenously formed angiotensin II influences this neurally mediated adrenal epinephrine release. The augmented release of epinephrine in rats maintained on the low-sodium diet appeared to depend on circulating angiotensin II because blockade of angiotensin II receptors with saralasin decreased the epinephrine release in these animals but not in rats maintained on the normal diet. Similar results were obtained when the renin-angiotensin system was blocked with the converting-enzyme inhibitor captopril. Adrenal epinephrine content was not affected by the dietary sodium intake; however, the catecholamine synthetic capacity was augmented as indicated by a significant induction of tyrosine hydroxylase. In addition, the adrenal medullary angiotensin II receptor density was significantly elevated in animals on the low-sodium diet. These results demonstrate that endogenous angiotensin II is capable of providing a positive modulatory influence on neurally mediated release of adrenal epinephrine, an effect that may require a chronic activation of the renin-angiotensin system as occurs naturally with restricted dietary sodium intake.


2012 ◽  
Vol 112 (6) ◽  
pp. 1049-1053 ◽  
Author(s):  
John H. Eisenach ◽  
Leah R. Gullixson ◽  
Susan L. Kost ◽  
Michael J. Joyner ◽  
Stephen T. Turner ◽  
...  

Dietary sodium and blood pressure regulation differs between normotensive men and women, an effect which may involve endothelial production of nitric oxide (NO). Therefore, we tested the hypothesis that differences in the NO component of endothelium-dependent vasodilation between low and high dietary sodium intake depend on sex. For 5 days prior to study, healthy adults consumed a controlled low-sodium diet (10 mmol/day, n = 30, mean age ± SE: 30 ± 1 yr, 16 men) or high-sodium diet (400 mmol/day, n = 36, age 23 ± 1 yr, 13 men). Forearm blood flow (FBF, plethysmography) responses to brachial artery administration of acetylcholine (ACh, 4 μg·100 ml tissue−1·min−1) were measured before and after endothelial NO synthase inhibition with NG-monomethyl-l-arginine (l-NMMA, 50 mg bolus + 1 mg/min infusion). The NO component of endothelium-dependent dilation was calculated as the response to ACh before and after l-NMMA accounting for changes in baseline FBF: [(FBF ACh − FBF baseline) − (FBF AChL-NMMA − FBF baselineL-NMMA)]. This value was 5.7 ± 1.3 and 2.5 ± 0.8 ml·100 ml forearm tissue−1·min−1 for the low- and high-sodium diets, respectively (main effect of sodium, P = 0.019). The sodium effect was larger for the men, with values of 7.9 ± 2.0 and 2.2 ± 1.4 for men vs. 3.1 ± 1.3 and 2.7 ± 1.0 ml·100 ml forearm tissue−1·min−1 for the women ( P = 0.034, sex-by-sodium interaction). We conclude that the NO component of endothelium-dependent vasodilation is altered by dietary sodium intake based on sex, suggesting that endothelial NO production is sensitive to dietary sodium in healthy young men but not women.


2015 ◽  
Vol 30 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Eloisa Colin-Ramirez ◽  
Finlay A. McAlister ◽  
Elizabeth Woo ◽  
Nellie Wong ◽  
Justin A. Ezekowitz

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