Mechanism of Cardiovascular Mortality During Low Sodium Diet: NO Bioavailability And The Renin Angiotensin‐NADPH Oxidase System

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Nobuhiro Suematsu ◽  
Caroline Ojaimi ◽  
Pawel M Kaminski ◽  
Zipping Wang ◽  
Xiaobin Xu ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Cardiovascular Mortality ◽  
Oxidase System ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
No Bioavailability

Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat

1980 ◽  
Vol 94 (3) ◽  
pp. 381-388 ◽  
Author(s):  
Eva Tarján ◽  
András Spät ◽  
Tamás Balla ◽  
Annamária Székely
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Sodium ◽  
Sodium Depletion ◽  
Angiotensin System ◽  
Aldosterone Level ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract. The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Rats were kept on control or low-sodium diet for one week. On the 7th morning of diet osmotic minipumps filled with the angiotensin converting enzyme inhibitor (CEI) SQ 20,881, or empty pumps, were implanted subcutaneously (sc). The rats were sacrificed 23 h later. Peripheral blood was analyzed for hormones and electrolytes. Adrenal capsular tissue (z. glomerulosa) was incubated for the determination of the conversion of [3H]corticosterone to [3H]aldosterone. Sodium depletion had no effect on plasma sodium, but it increased potassium concentration. Infusion of CEI had no significant effect on plasma electrolytes. Plasma renin activity was increased both by sodium depletion and CEI. The mean serum aldosterone level was twelve times higher in sodium depleted animals than in controls. Aldosterone level was reduced by about 60 per cent in CEI-infused animals both on control and low-sodium diet. The conversion of corticosterone to aldosterone was significantly stimulated by sodium deprivation. This effect was also inhibited by the CEI SQ 20,881.

Angiotensin augments epinephrine release in pithed rats fed a low-sodium diet

1990 ◽  
Vol 258 (1) ◽  
pp. R187-R192 ◽  
Author(s):  
R. R. Vollmer ◽  
S. P. Corey ◽  
S. A. Meyers ◽  
E. M. Stricker ◽  
S. J. Fluharty
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Dietary Sodium ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Pithed Rats

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.

Endothelial function during stimulation of renin-angiotensin system by low-sodium diet in humans

2001 ◽  
Vol 280 (5) ◽  
pp. H2248-H2254 ◽  
Author(s):  
Torbjørn Omland ◽  
Wendy Johnson ◽  
Mary Beth Gordon ◽  
Mark A. Creager
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Concomitant Treatment ◽  
Double Blind ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Stimulation Of

We examined whether physiological stimulation of the endogenous renin-angiotensin system results in impaired endothelium-dependent vasodilatation in forearm resistance vessels of healthy subjects and whether this impairment can be prevented by angiotensin II type 1 receptor blockade. A low-sodium diet was administered to 27 volunteers who were randomized to concomitant treatment with losartan (100 mg once daily) or matched placebo in a double-blind fashion. Forearm blood flow was assessed by venous occlusion plethysmography at baseline and after 5 days. Endothelium-dependent and -independent vasodilation was assessed by intra-arterial infusion of methacholine and verapamil, respectively. The low-sodium diet resulted in significantly decreased urine sodium excretion (placebo: 146 ± 64 vs. 10 ± 9 meq/24 h, P < 0.001; losartan: 141 ± 56 vs. 14 ± 14 meq/24 h, P < 0.001) and increased plasma renin activity (placebo: 1.0 ± 0.5 vs. 5.0 ± 2.5 ng · ml−1 · h−1, P < 0.001; losartan: 3.8 ± 7.2 vs. 19.1 ± 11.2 ng · ml−1 · h−1, P = 0.006) in both the losartan and placebo groups. With the baseline study as the reference, the diet intervention was not associated with any significant change in endothelium-dependent vasodilation to methacholine in either the placebo ( P = 0.74) or losartan ( P = 0.40) group. We conclude that short-term physiological stimulation of the renin-angiotensin system does not cause clinically significant endothelial dysfunction. Losartan did not influence endothelium-dependent vasodilation in humans with a stimulated renin-angiotensin system.

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.

Sign in / Sign up

Export Citation Format

Share Document