Hindbrain mineralocorticoid mechanisms on sodium appetite

2013 ◽  
Vol 304 (3) ◽  
pp. R252-R259 ◽  
Author(s):  
Silmara Formenti ◽  
Mirian Bassi ◽  
Natália B. Nakamura ◽  
Guus H. M. Schoorlemmer ◽  
José V. Menani ◽  
...  
Keyword(s):  
Daily Intake ◽  
Sodium Diet ◽  
Sodium Appetite ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Chronic Infusion ◽  
Male Wistar Rats ◽  
Ru 28318 ◽  
Acute Injection ◽  
Powerful Mechanism

Aldosterone acting on the brain stimulates sodium appetite and sympathetic activity by mechanisms that are still not completely clear. In the present study, we investigated the effects of chronic infusion of aldosterone and acute injection of the mineralocorticoid receptor (MR) antagonist RU 28318 into the fourth ventricle (4th V) on sodium appetite. Male Wistar rats (280–350 g) with a stainless-steel cannula in either the 4th V or lateral ventricle (LV) were used. Daily intake of 0.3 M NaCl increased to 46 ± 15 and 130 ± 6 ml/24 h after 6 days of infusion of 10 and 100 ng/h of aldosterone into the 4th V (intake with vehicle infusion: 2 ± 1 ml/24 h). Water intake fell slightly and not consistently, and food intake was not affected by aldosterone. Sodium appetite induced by diuretic (furosemide) combined with 24 h of a low-sodium diet fell from 12 ± 1.7 ml/2 h to 5.6 ± 0.8 ml/2 h after injection of the MR antagonist RU 28318 (100 ng/2 μl) into the 4th V. RU 28318 also reduced the intake of 0.3 M NaCl induced by 9 days of a low-sodium diet from 9.5 ± 2.6 ml/2 h to 1.2 ± 0.6 ml/2 h. Infusion of 100 or 500 ng/h of aldosterone into the LV did not affect daily intake of 0.3 M NaCl. The results are functional evidence that aldosterone acting on MR in the hindbrain activates a powerful mechanism involved in the control of sodium appetite.

The Role of Angiotensin II on Sodium Appetite After a Low-Sodium Diet

2013 ◽  
Vol 25 (3) ◽  
pp. 281-291 ◽  
Author(s):  
A. S. Mecawi ◽  
T. Vilhena-Franco ◽  
F. V. Fonseca ◽  
L. C. Reis ◽  
L. L. K. Elias ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Diet ◽  
Sodium Appetite ◽  
Low Sodium Diet ◽  
Low Sodium

Time for a Renewed Focus on the DASH-Low Sodium Diet

2021 ◽  
Vol 77 (21) ◽  
pp. 2635-2637
Author(s):  
Neha J. Pagidipati ◽  
Laura P. Svetkey
Keyword(s):  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Taste Perception in Three Individuals on a Low Sodium Diet

Appetite ◽  
1981 ◽  
Vol 2 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Mary Bertino ◽  
G.K. Beauchamp ◽  
D.R. Riskey ◽  
K. Engelman
Keyword(s):  
Taste Perception ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract 17541: An Education Intervention Focused on Self-monitoring for Symptom and Sodium Intake Improves Adherence to the Low Sodium Diet and Health Outcome in Patients with Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eun Kyeung Song ◽  
Debra K Moser ◽  
Seok-Min Kang ◽  
Terry A Lennie
Keyword(s):  
Health Outcomes ◽  
Cox Regression ◽  
Sodium Intake ◽  
Control Group ◽  
Education Intervention ◽  
Self Monitoring ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Patients With Heart Failure

Background: Despite the clinical emphasis on recommending a low sodium diet (LSD), adherence to a LSD remains poor in patients with heart failure (HF). Additional research is needed to determine successful interventions to improve adherence to a LSD and health outcomes. Purpose: To determine the effect of an education intervention on adherence to a LSD and health outcomes. Method: A total of 109 HF patients (age 64±9 years, 29% female) who were non-adherent to LSD, indicating > 3g of 24-hour urinary sodium excretion (24hr UNa) at baseline, were randomly assigned to one of 3 groups: 1) symptom monitoring and restricted 3 gram sodium diet (SMART) group, 2) the telephone monitoring (TM) group, or 3) usual care control group. The SMART group received individualized teaching and guidance of self-monitoring for worsening symptom and sodium intake using symptom and food diary for 4 sessions over 8 weeks. Patients assigned to either of the 2 intervention groups (SMART or TM) received phone calls every 2 weeks over 8 weeks. At 6 months follow-up, adherence to a LSD was assessed using 24hr UNa. Patients were followed for 1 year to determine time to first event of hospitalization or death due to cardiac problems. Repeated measures ANOVA and Cox regression were used to determine the effect of intervention. Results: The SMART group (n=37) showed a significant reduction in sodium intake across time compared to the TM group (n=35) and control group (n=37) (p= .022). In the Cox regression, patients in the SMART group had longer cardiac event-free survival compared to the control group after controlling for age, gender, ejection fraction, angiotensin-converting enzyme inhibitor use, and better blocker use (p=.008). Conclusion: An education intervention focused on self-monitoring for symptom and sodium intake improved adherence to LSD and health outcomes in patients with HF. Helping patients engage in self-monitoring for symptom and sodium intake by themselves can promote better health outcome.

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.

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