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 ◽  
...  

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.

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.


Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Mohammed MIMOUNI ◽  
Solene DARLET ◽  
Bernard F JOVER ◽  
Laura JEANSON ◽  
Marie-Pierre BLANCHARD ◽  
...  

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.


1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah

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.


1990 ◽  
Vol 124 (3) ◽  
pp. 507-513 ◽  
Author(s):  
E. A. P. Steegers ◽  
Th. J. Benraad ◽  
H. W. Jongsma ◽  
A. C. I. T. L. Tan ◽  
P. R. Hein

ABSTRACT The effects of dietary sodium restriction and posture on plasma concentrations of atrial natriuretic peptide (ANP), aldosterone and free aldosterone were investigated in ten women between weeks 29 and 33 of normal pregnancy. Hormone levels were studied during unrestricted sodium intake and on day 6 of a low sodium diet. On both occasions venous blood was obtained in the sitting as well as in the left lateral tilt position. Plasma concentrations of ANP during the unrestricted sodium intake were not raised compared with control values in healthy non-pregnant females. Recovery experiments showed no differences in the degradation of ANP in blood from pregnant and non-pregnant women. Plasma concentrations of ANP significantly decreased (by 32%) in response to the low sodium regime in both positions. Concentrations of aldosterone and free aldosterone (in women in the sitting position) increased twofold after sodium restriction. Mean values of ANP were higher in women in the left lateral tilt position that in those in the sitting position, but the difference was not significant. Concentrations of aldosterone and free aldosterone were significantly lower (by around 30%) in women in the left lateral tilt position compared with those in the sitting posture. Journal of Endocrinology (1990) 124, 507–513


2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Emma J. McMahon ◽  
Katrina L. Campbell ◽  
David W. Mudge ◽  
Judith D. Bauer

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.


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.


1983 ◽  
Vol 245 (3) ◽  
pp. F322-F328 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin

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.


1985 ◽  
Vol 249 (6) ◽  
pp. F819-F826 ◽  
Author(s):  
E. Fernandez-Repollet ◽  
C. R. Silva-Netto ◽  
R. E. Colindres ◽  
C. W. Gottschalk

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.


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