Renal nerves in renal adaptation to dietary sodium restriction

1983 ◽  
Vol 245 (3) ◽  
pp. F322-F328 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Renal Denervation ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Body Sodium ◽  
Renal Adaptation

To assess the physiologic importance of the renal nerves in the renal mechanisms for the maintenance of body sodium balance, renal adaptation to normal and low sodium diet was evaluated in conscious Sprague-Dawley male rats before and 8 days after recovery from bilateral surgical-pharmacological renal denervation. Renal denervation was confirmed in every rat at the end of the study by absence of renal vasoconstriction to splanchnic nerve stimulation and loss of renal tissue norepinephrine content. Daily sodium balance, defined as the difference between dietary sodium intake and urinary sodium excretion, was positive with the normal sodium diet before and after bilateral renal denervation. Prior to bilateral renal denervation, changing to the low sodium diet was associated with a diminishingly negative sodium balance for 3 days that became progressively positive thereafter. After bilateral renal denervation, changing to the low sodium diet was associated with a continuous and progressively negative sodium balance. We conclude that intact renal innervation is required for normal renal sodium conservation and maintenance of body sodium balance during dietary sodium restriction.

Role of renal nerves in maintaining sodium balance in unrestrained conscious rats

1985 ◽  
Vol 249 (6) ◽  
pp. F819-F826 ◽  
Author(s):  
E. Fernandez-Repollet ◽  
C. R. Silva-Netto ◽  
R. E. Colindres ◽  
C. W. Gottschalk
Keyword(s):  
Blood Pressure ◽  
Renal Denervation ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Low Sodium ◽  
Dietary Sodium Restriction

This study was designed to investigate the effects of bilateral renal denervation on sodium and water balance, the renin-angiotensin system, and systemic blood pressure in unrestrained conscious rats maintained on a normal- or low-sodium diet. Renal denervation was proven by chemical and functional tests. Both bilaterally denervated rats (n = 18) and sham-denervated rats (n = 15) maintained positive sodium balance while on a normal sodium intake. Both groups were in negative sodium balance for 1 day after dietary sodium restriction was instituted but were in positive sodium balance for the following 9 days. Systolic blood pressure was higher in sham-denervated (115 +/- 3 mmHg) than in denervated rats (102 +/- 3 mmHg) while on a normal diet (P less than 0.05) and remained so during sodium restriction. Plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) were significantly diminished in the denervated rats during normal sodium intake (P less than 0.05). After dietary sodium restriction, PRC increased in both groups but remained significantly lower in the denervated rats (P less than 0.05). Following dietary sodium restriction, PAC also increased significantly to levels that were similar in both groups of rats. These results demonstrate that awake unrestrained growing rats can maintain positive sodium balance on a low sodium intake even in the absence of the renal nerves. However, efferent renal nerve activity influenced plasma renin activity in these animals.

Development of two-kidney Goldblatt hypertension in rats under dietary sodium restriction

1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Goldblatt Hypertension

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.

Adrenergic control of renin during dietary sodium deprivation in conscious dogs

1989 ◽  
Vol 256 (6) ◽  
pp. E863-E871 ◽  
Author(s):  
H. Hisa ◽  
Y. H. Chen ◽  
K. J. Radke ◽  
J. L. Izzo ◽  
C. D. Sladek ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Conscious Dogs ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Adrenergic Stimulation ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Dietary Sodium Restriction

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.

Abstract P163: Prevention Of Cardiac Fibrosis By Dietary Sodium Restriction During Metabolic Syndrome: Involvement Of Endothelial To Mesenchymal Transition

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Mohammed MIMOUNI ◽  
Solene DARLET ◽  
Bernard F JOVER ◽  
Laura JEANSON ◽  
Marie-Pierre BLANCHARD ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
Cardiac Fibrosis ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Mesenchymal Transition ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Dietary Sodium Restriction

In a rat model of metabolic syndrome (MS), our previous studies have shown that dietary sodium restriction prevents both metabolic and cardiac damages associated with MS. Our aim is now to investigate whether the beneficial effects of sodium restriction could be mediated by endothelial to mesenchymal (EndoMT) transition in the myocardium thereby preventing cardiac fibrosis.High fructose (60%) Sprague Dawley rats were divided into 2 groups: low sodium (<0.01% NaCl, N=20) or normal sodium (0.65% NaCl, N=20) diet for 8 weeks. EndoMT was investigated by q-PCR, WB, and IF on the left ventricles. Transcriptomic analysis was performed using Agilent Rat Gene Expression Microarray. After 8 weeks, fructose-fed rats on normal sodium diet were insulin-resistant and hypertensive, both abnormalities being significantly prevented by sodium restriction. In left ventricles, two mesenchymal proteins, α-smooth muscle actin (αSMA) and vimentin were found significantly reduced using qPCR and WB by sodium restriction (P<0.05), as compared to normal sodium diet. At the opposite, we observed a significant increase in Pecam-1, a specific protein of vascular endothelial cells (P<0.05). Using IF, we detected a co-expression of αSMA and Pecam-1 in 67.3%±4.9 (54 of 88) of cardiac vessels of rats fed normal sodium diet, as compared to 42.3%±3.8 (37 of 88) in rats fed low sodium diet (P<0.05). The transcriptomic study showed that 22 genes, involved in fibrosis, were down-regulated in left ventricles of sodium-restricted rats (P<0.05). By q-PCR, we confirmed that 17 of them were significantly reduced by the low sodium diet (P<0.05). Finally, we established an in vitro model of EndoMT, using primary human aortic endothelial (HAoE) cells that were transdifferentiated with TGF-β2 (10ng/ml). We evidenced in HAoE cells the co-expression of Pecam-1 and collagen-1, as a signature of EndoMT. Especially, fibulin 5, one of the genes identified by transcriptomics was found upregulated (13 folds) in the presence of TGF-β2, confirming its potential role in EndoMT. Our study shows that EndoMT is involved in the prevention of cardiac fibrosis by sodium restriction in our rat model of MS. We also confirmed the involvement of ew genes that could be of interest to improve the management of cardiac fibrosis.

Dietary Sodium Restriction in Normotensive Subjects and Patients with Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 399s-402s ◽  
Author(s):  
G. A. MacGregor ◽  
N. D. Markandu ◽  
G. A. Sagnella
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Normal Diet ◽  
Mean Blood Pressure ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Normotensive Subjects

1. Seventy-seven patients with essential hypertension and 28 normotensive subjects were studied on their normal diet (ND), on the fifth day of a high sodium diet (HS) (350 mmol/day) and on the fifth day of a low sodium diet (LS) (10 mmol/day). 2. With an increase in sodium intake, there was no change in mean blood pressure either in the normotensive subjects (ND, 120/75 ± 2.4/1.7 mmHg—HS, 119/75 ± 2.7/1.7 mmHg) or in the hypertensive subjects (ND, 173/110 ± 2.5/1.3 mmHg—HS, 174/110 ± 2.5/1.4 mmHg). 3. On the fifth day of the low sodium diet there was no change in mean blood pressure in the normotensive subjects (ND, 120/75 ± 2.5/1.7 mmHg—LS, 116/76 ± 2.7/2.0 mmHg). In contrast, the hypertensive group on the fifth day of the low salt diet had a significant fall in supine mean blood pressure compared with those on the normal diet (ND, 173/110 ± 2.5/1.3—LS, 155/102 ± 2.2/1.3 mmHg; P < 0.001). The fall in mean blood pressure was 10.8 ± 1.1 mmHg (8.4%). 4. There was a significant correlation between the fall in blood pressure with the low sodium diet and the level of blood pressure on the normal diet (r = 0.52; P < 0.001) and a significant inverse correlation with the fall in blood pressure on the low sodium diet and the rise in plasma renin activity from the normal to low sodium diet (r = −0.36; P < 0.001). 5. Nineteen patients with mild to moderate essential hypertension were studied in a double-blind randomized crossover study of moderate dietary sodium restriction using slow sodium and placebo for 1 month each. On the fourth week of placebo (mean 24 h UNa 86 ± 9 mmol), mean supine blood pressure was 7.1 mmHg lower (6.1%), P < 0.001 compared with the fourth week of slow sodium (mean 24 h UNa 162 ± 9 mmol). 6. Moderate dietary sodium restriction over 1 month caused a fall in blood pressure in patients with essential hypertension. A more severe reduction in sodium intake for a shorter period of time lowered blood pressure in hypertensive but not normotensive subjects. Part of the mechanism of this blood pressure reduction with sodium restriction appeared to be related to the severity of the hypertension and to suppression of the renin-angiotensin system.

Role of renal nerves in renal sodium retention of nephrotic syndrome

1989 ◽  
Vol 256 (5) ◽  
pp. F823-F829 ◽  
Author(s):  
P. J. Herman ◽  
L. L. Sawin ◽  
G. F. DiBona
Keyword(s):  
Nephrotic Syndrome ◽  
Renal Denervation ◽  
Sodium Content ◽  
Vehicle Control ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Retention ◽  
Edema Formation

To define the role of the renal nerves in the renal sodium retention of the nephrotic syndrome, experiments were conducted in rats given adriamycin to produce nephrotic syndrome. All rats developed proteinuria and hypoalbuminemia and exhibited edema formation. Adriamycin-injected nephrotic rats were subjected to bilateral renal denervation (ADRIADNX) or sham renal denervation (ADRIASHAM). Rats injected with adriamycin vehicle were subjected to bilateral renal denervation (DNX) or sham renal denervation (SHAM). Metabolic balance studies were carried out in all rats beginning on the 8th day after bilateral or sham renal denervation. Dietary sodium content was 210 meq/kg Na on days 8-12 and days 24-26 and was 10 meq/kg Na on days 13-23. Nephrotic rats demonstrated significantly greater overall (19 days) cumulative sodium balance than vehicle control rats, ADRIASHAM 8.47 +/- 0.81 vs. SHAM 5.74 +/- 0.34 meq Na, P less than 0.01. Bilateral renal denervation did not significantly affect overall cumulative sodium balance in the vehicle control rats, DNX 6.15 +/- 0.71 vs. SHAM 5.74 +/- 0.34 meq Na. However, bilateral renal denervation significantly decreased overall cumulative sodium balance in the nephrotic rats, ADRIADNX 6.59 +/- 0.56 vs. ADRIASHAM 8.47 +/- 0.81 meq Na, P less than 0.01. Results indicated that the increased renal sodium retention characteristic of nephrotic syndrome is dependent, in large part, on increased efferent renal sympathetic nerve activity.

scholarly journals Achieving Salt Restriction in Chronic Kidney Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Emma J. McMahon ◽  
Katrina L. Campbell ◽  
David W. Mudge ◽  
Judith D. Bauer
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Sodium Intake ◽  
Epidemiological Studies ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Restricted Diet ◽  
Salt Restriction ◽  
Low Sodium Diet ◽  
Low Sodium

There is consistent evidence linking excessive dietary sodium intake to risk factors for cardiovascular disease and chronic kidney disease (CKD) progression in CKD patients; however, additional research is needed. In research trials and clinical practice, implementing and monitoring sodium intake present significant challenges. Epidemiological studies have shown that sodium intake remains high, and intervention studies have reported varied success with participant adherence to a sodium-restricted diet. Examining barriers to sodium restriction, as well as factors that predict adherence to a low sodium diet, can aid researchers and clinicians in implementing a sodium-restricted diet. In this paper, we critically review methods for measuring sodium intake with a specific focus on CKD patients, appraise dietary adherence, and factors that have optimized sodium restriction in key research trials and discuss barriers to sodium restriction and factors that must be considered when recommending a sodium-restricted diet.

scholarly journals Evidence related to sodium restriction in patients with heart failure

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 ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sodium Intake ◽  
Main Tool ◽  
Dietary Sodium ◽  
Protective Measure ◽  
Sodium Restriction ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Asymptomatic Patients ◽  
Patients With Heart Failure

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.

PATHOPHYSIOLOGICAL CHANGES IN PLASMA AND BODY COMPSITION OF YOUNG POULTS FED A SODIUM-DEFICIENT DIET

1978 ◽  
Vol 58 (4) ◽  
pp. 597-604
Author(s):  
C. Y. PANG ◽  
L. D. CAMPBELL ◽  
G. D. PHILLIPS
Keyword(s):  
Tap Water ◽  
Basal Diet ◽  
Plasma Sodium ◽  
Deficient Diet ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Body Sodium ◽  
Ad Libitum ◽  
Water Contents

Significantly lower feed intake, higher water intake and depressed growth rate were observed in poults under 30 days of age offered ad libitum a low (0.05%) sodium diet and tap water compared to control poults offered the same basal diet containing 0.25% added sodium. Mortality with dehydration occurred mainly between 2 and 3 wk of age in poults fed the low sodium diet. Significant pathophysiological changes in poults fed low sodium diet compared with the control on days 9–30 were: lower plasma sodium, chloride and osmolal concentrations; higher plasma contents of uric acid and total protein; higher packed cell volume; and lower body sodium and water contents. Indications of extracellular dehydration and intracellular hydration and decreased glomerular filtration rate in sodium-deficient poults are discussed. Plasma and body composition of poults fed the low sodium diet returned to normal 1 wk after the poults were offered a normal (0.25%) sodium diet and tap water ad libitum.

Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1–7) administration in anesthetized rats

2013 ◽  
Vol 304 (3) ◽  
pp. R260-R266 ◽  
Author(s):  
Julie O'Neill ◽  
Alan Corbett ◽  
Edward J. Johns
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Hemodynamic

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.

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