Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?

2008 ◽  
Vol 114 (3) ◽  
pp. 221-230 ◽  
Author(s):  
Salvatore Paterna ◽  
Parrinello Gaspare ◽  
Sergio Fasullo ◽  
Filippo M. Sarullo ◽  
Pietro Di Pasquale
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Heart Association ◽  
Plasma Renin ◽  
High Dose ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Significant Difference

The aim of the present study was to evaluate the effects of a normal-sodium (120 mmol sodium) diet compared with a low-sodium diet (80 mmol sodium) on readmissions for CHF (congestive heart failure) during 180 days of follow-up in compensated patients with CHF. A total of 232 compensated CHF patients (88 female and 144 male; New York Heart Association class II–IV; 55–83 years of age, ejection fraction <35% and serum creatinine <2 mg/dl) were randomized into two groups: group 1 contained 118 patients (45 females and 73 males) receiving a normal-sodium diet plus oral furosemide [250–500 mg, b.i.d. (twice a day)]; and group 2 contained 114 patients (43 females and 71 males) receiving a low-sodium diet plus oral furosemide (250–500 mg, b.i.d.). The treatment was given at 30 days after discharge and for 180 days, in association with a fluid intake of 1000 ml per day. Signs of CHF, body weight, blood pressure, heart rate, laboratory parameters, ECG, echocardiogram, levels of BNP (brain natriuretic peptide) and aldosterone levels, and PRA (plasma renin activity) were examined at baseline (30 days after discharge) and after 180 days. The normal-sodium group had a significant reduction (P<0.05) in readmissions. BNP values were lower in the normal-sodium group compared with the low sodium group (685±255 compared with 425±125 pg/ml respectively; P<0.0001). Significant (P<0.0001) increases in aldosterone and PRA were observed in the low-sodium group during follow-up, whereas the normal-sodium group had a small significant reduction (P=0.039) in aldosterone levels and no significant difference in PRA. After 180 days of follow-up, aldosterone levels and PRA were significantly (P<0.0001) higher in the low-sodium group. The normal-sodium group had a lower incidence of rehospitalization during follow-up and a significant decrease in plasma BNP and aldosterone levels, and PRA. The results of the present study show that a normal-sodium diet improves outcome, and sodium depletion has detrimental renal and neurohormonal effects with worse clinical outcome in compensated CHF patients. Further studies are required to determine if this is due to a high dose of diuretic or the low-sodium diet.

scholarly journals A Low-Sodium Diet Boosts Ang (1–7) Production and NO-cGMP Bioavailability to Reduce Edema and Enhance Survival in Experimental Heart Failure

2021 ◽  
Vol 22 (8) ◽  
pp. 4035
Author(s):  
Ranjana Tripathi ◽  
Ryan D. Sullivan ◽  
Tai-Hwang M. Fan ◽  
Radhika M. Mehta ◽  
Inna P. Gladysheva ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Systolic Function ◽  
Plasma Renin ◽  
Guanosine Monophosphate ◽  
Cgmp Production ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Nitric Oxide Bioavailability

Sodium restriction is often recommended in heart failure (HF) to block symptomatic edema, despite limited evidence for benefit. However, a low-sodium diet (LSD) activates the classical renin-angiotensin-aldosterone system (RAAS), which may adversely affect HF progression and mortality in patients with dilated cardiomyopathy (DCM). We performed a randomized, blinded pre-clinical trial to compare the effects of a normal (human-equivalent) sodium diet and a LSD on HF progression in a normotensive model of DCM in mice that has translational relevance to human HF. The LSD reduced HF progression by suppressing the development of pleural effusions (p < 0.01), blocking pathological increases in systemic extracellular water (p < 0.001) and prolonging median survival (15%, p < 0.01). The LSD activated the classical RAAS by increasing plasma renin activity, angiotensin II and aldosterone levels. However, the LSD also significantly up-elevated the counter-regulatory RAAS by boosting plasma angiotensin converting enzyme 2 (ACE2) and angiotensin (1–7) levels, promoting nitric oxide bioavailability and stimulating 3′-5′-cyclic guanosine monophosphate (cGMP) production. Plasma HF biomarkers associated with poor outcomes, such as B-type natriuretic peptide and neprilysin were decreased by a LSD. Cardiac systolic function, blood pressure and renal function were not affected. Although a LSD activates the classical RAAS system, we conclude that the LSD delayed HF progression and mortality in experimental DCM, in part through protective stimulation of the counter-regulatory RAAS to increase plasma ACE2 and angiotensin (1–7) levels, nitric oxide bioavailability and cGMP production.

Low-Sodium Diet and Free Fluid Intake in the Treatment of Congestive Heart Failure

1946 ◽  
Vol 234 (18) ◽  
pp. 573-578 ◽  
Author(s):  
William C. Bridges ◽  
Edwin O. Wheeler ◽  
Paul D. White
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Fluid Intake ◽  
Free Fluid ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract 16922: Feasibility of Family Sodium Watcher Program to Improve Adherence to Low Sodium Diet in Patients with Heart Failure and Caregivers

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Misook L Chung ◽  
Debra K Moser ◽  
Terry A Lennie
Keyword(s):  
Heart Failure ◽  
Rating Scale ◽  
Intervention Group ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Point Rating Scale ◽  
Patients With Heart Failure ◽  
Monitoring Devices

Introduction: Poor adherence to the low sodium diet (LSD), common in patients with heart failure (HF), is a major predictor of hospitalization for exacerbation of HF. When family member’s consume the same LSD recommended for patients, patient adherence is increased. The Sodium Watcher Program (SWAP) was developed to improve adherence to LSD using a gradual adaptation strategy and an electronic salt monitoring device that allows detection of sodium content in food. The purpose of this study was to examine whether the SWAP was feasible and if it resulted in reduction in sodium intake for patients with HF and their caregivers. Method: In this 2-group randomized controlled trial, 15 patient-caregiver dyads completed 24-hour urine collection for sodium excretion level (24h UNa) at baseline and 3 months follow up. Dyads in the SWAP intervention (n=8) received 12 weeks of self-care education for HF and LSD with gradual adaptation strategies in salt intake via 2 home visits and 4 calls. Paired t-test was used to compare adherence to LSD at two data collection times. Only intervention group evaluated use of the electronic salt monitoring devices and the intervention program at 3 months. Results: The intervention group had a significant reduction in 24h UNa (Patients 3894mg vs. 3604mg, p=.02; caregivers 4123mg vs. 3380mg, p<.05). They also reported significant increased level of enjoying eating LSD (M =5.4 on 10-point rating scale vs. M=7.9 p <.01) and 90% noticed a change in their ability to taste salt in their food at the 3-month follow up. They reported that use of the electronic monitoring devices was easy (M=8.3 on 10-point rating scale) and helpful in supporting LSD adherence (M=8.8 on 10-point rating scale). Caregivers in the intervention reported no significant changes in burden levels. The usual care control group had no change in 24h UNa (patients 4369 mg vs. 4434 mg; caregivers 3301 mg vs. 4826mg). Conclusion: The findings demonstrated that the SWaP is feasible and efficacious for following LSD by dyads. The intervention was feasible for caregivers and did not increase caregiver burden. This family intervention may have potential for promoting long-term adherence and needs to be tested in a larger clinical trial.

Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion

1987 ◽  
Vol 253 (1) ◽  
pp. R179-R185
Author(s):  
E. Gotoh ◽  
K. Murakami ◽  
T. D. Bahnson ◽  
W. F. Ganong
Keyword(s):  
Plasma Renin ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Renin Secretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Head Up Tilt ◽  
Dorsal Raphé

To investigate the role of brain serotonergic neurons in the regulation of renin secretion, we measured changes in plasma renin activity (PRA), and, in some instances, plasma renin concentration (PRC), plasma angiotensinogen, and plasma adrenocorticotropic hormone (ACTH) in rats with lesions of the dorsal raphe nucleus and lesions of the paraventricular nuclei, dorsomedial nuclei, and ventromedial nuclei of the hypothalamus. We also investigated the effects of p-chloroamphetamine (PCA), immobilization, head-up tilt, and a low-sodium diet in the rats with dorsal raphe, paraventricular, and dorsomedial lesions. Lesions of the dorsal raphe nucleus abolished the increase in PRA produced by PCA but had no effect on the increase produced by immobilization, head-up tilt, and a low-sodium diet. Paraventricular lesions, which abolish the increase in plasma ACTH produced by PCA, immobilization, and head-up tilt, decreased plasma angiotensinogen. The paraventricular lesions abolished the PRA and the PRC responses to PCA and the PRA but not PRC response to immobilization, head-up tilt, and a low-sodium diet. The ventromedial lesions abolished the PRA and PRC responses to PCA and did not reduce plasma angiotensinogen. The data suggest that paraventricular lesions depress angiotensinogen production by the liver and that the paraventricular and ventromedial nuclei are part of the pathway by which serotonergic discharges increase renin secretion. They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet.

Hypotensive effect of [Sar1,Thr8]angiotensin II in spontaneously hypertensive sodium-depleted rats

1978 ◽  
Vol 234 (4) ◽  
pp. H447-H453
Author(s):  
H. Munoz-Ramirez ◽  
M. C. Khosla ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Normal Diet ◽  
Spontaneously Hypertensive ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Angiotensin Ii Antagonist

Under inactin anesthesia, intravenous infusion of [Sar1,Thr8]angiotensin II produced a hypotensive effect in young spontaneously hypertensive rats (SHR) treated with furosemide and in mature SH rats fed a low-sodium diet. The angiotensin antagonist also lowered blood pressure of young and mature SH rats receiving a normal diet. Deoxycorticosterone acetate (DOCA) plus saline reversed the hypotensive effect of [Saru,Thr8]angiotensin II in young SH rats, but did not do so in mature SH rats. Plasma renin activity (PRA) was not significantly changed by anesthesia. Furosemide or the low-sodium diet significantly increased PRA in young and mature SH rats. In contrast, DOCA plus saline significantly reduced PRA in both young and mature SH rats. However, there was no correlation between PRA and the action of the angiotensin II antagonist. These data suggest that the renin-angiotensin system is involved in genetic hypertension.

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