A Comparison of Natriuresis after Oral and Intravenous Sodium Loading in Sodium-Depleted Man: Evidence for a Gastrointestinal or Portal Monitor of Sodium Intake

1975 ◽  
Vol 49 (5) ◽  
pp. 437-440 ◽  
Author(s):  
R. J. Lennane ◽  
R. M. Carey ◽  
T. J. Goodwin ◽  
W. S. Peart
Keyword(s):  
Gastrointestinal Tract ◽  
Early Recognition ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Compensatory Response ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Portal Monitor ◽  
The Difference ◽  
Intravenous Sodium

1. Dietary sodium reduction in man is followed by rapid conservation of sodium by the kidneys. The rapidity of this response suggests that the gastrointestinal tract is involved in early recognition of changes in sodium intake or in mediation of the compensatory response. 2. In order to test the hypothesis, 100 mmol of sodium was given to normal volunteers in balance on a low-sodium diet (5 mmol/24 h): the dose was given either orally or intravenously. 3. Those who received their sodium orally excreted it more rapidly than those who received it intravenously and the difference was most marked in the first 8 h after the dose. 4. This finding is consistent with the presence of an input receptor for sodium in the gastrointestinal tract.

A Comparison of Natriuresis after Oral and Intravenous Sodium Loading in Sodium-Depleted Rabbits: Evidence for a Gastrointestinal or Portal Monitor of Sodium Intake

1975 ◽  
Vol 49 (5) ◽  
pp. 433-436 ◽  
Author(s):  
R. J. Lennane ◽  
W. S. Peart ◽  
R. M. Carey ◽  
J. Shaw
Keyword(s):  
Sodium Chloride ◽  
Sodium Intake ◽  
Portal Circulation ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sodium Loading ◽  
Portal Monitor ◽  
Oral Doses ◽  
Intravenous Sodium

1. Rabbits in balance on a low sodium diet were given doses of sodium chloride either orally or intravenously. 2. Those receiving oral doses responded with a much greater natriuresis than those receiving intravenous ones. 3. This could be explained by the existence of a sodium input monitor somewhere in the gut or portal circulation.

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.

Sodium Excretion in Man, and Adaptation to a Low-Sodium Diet: Effect of Intravenous Sodium Chloride

1979 ◽  
Vol 57 (3) ◽  
pp. 225-231 ◽  
Author(s):  
D. Gordon ◽  
W. S. Peart
Keyword(s):  
Sodium Chloride ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Plasma Sodium ◽  
Normal Male ◽  
Renal Sodium Excretion ◽  
Portal Monitor ◽  
Intravenous Sodium ◽  
Oral Sodium

1. The aim of this study was to test whether a postulated gastrointestinal or portal monitor of sodium intake plays any part in adjusting renal sodium excretion when dietary sodium is reduced. 2. Normal male subjects were given 50 mmol of sodium chloride intravenously three times daily for 3 days to replace or to supplement a constant oral intake of sodium chloride. 3. When oral sodium chloride was replaced with intravenous sodium chloride, renal sodium excretion remained constant. 4. When oral sodium chloride was kept constant, sodium administered as intravenous sodium chloride was promptly excreted in three out of four subjects. There was a delay in the increase in sodium excretion in the fourth subject. 5. Infusions containing 50 mmol of sodium chloride in 50 ml given intravenously over 22 min produced a rise in plasma sodium concentration and a fall in concentration of total plasma solids. 6. These results provide no evidence for a gastrointestinal or portal monitor of sodium intake, but do not disprove the existence of such a monitor.

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.

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.

Long-Term Adherence to Low-Sodium Diet in Patients With Heart Failure

2017 ◽  
Vol 39 (4) ◽  
pp. 553-567 ◽  
Author(s):  
Misook L. Chung ◽  
Linda Park ◽  
Susan K. Frazier ◽  
Terry A. Lennie
Keyword(s):  
Heart Failure ◽  
Patient Adherence ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Factors Affecting ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Positive Attitudes

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.

Gastrointestinal control of sodium excretion in sodium-depleted conscious rabbits

1976 ◽  
Vol 230 (6) ◽  
pp. 1504-1508 ◽  
Author(s):  
RM Carey ◽  
Smith ◽  
EM Ortt
Keyword(s):  
Gastrointestinal Tract ◽  
Sodium Excretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Sodium Excretion ◽  
Sodium Loading ◽  
Conscious Rabbits ◽  
Intravenous Sodium ◽  
Oral Sodium

Recent studies of sodium-depleted rabbits have shown that oral sodium loading is followed by greater natriuresis than intravenous sodium loading. The present study was undertaken to determine if this is dependent on differences in aldosterone excretion. Rabbits in balance on a low-sodium diet were given bolus doses of sodium either orally or intravenously. Those receiving oral sodium responded with a greater natriuresis than those receiving it intravenously. No differences in aldosterone excretion were demonstrated after oral or intravenous sodium repletion. Rabbits given large doses of exogenous aldosterone continued to excrete more sodium after oral than after intravenous repletion. This study demonstrates that in rabbits the gastrointestinal tract functions to regulate renal sodium excretion and that the mechanism is independent of aldosterone.

scholarly journals Diminished Antiproteinuric Effect Of The Angiotensin Receptor Blocker Losartan During High Potassium Intake In Patients With Ckd

2021 ◽  
Author(s):  
Rosa D Wouda ◽  
Femke Waanders ◽  
Dick de Zeeuw ◽  
Gerjan Navis ◽  
Liffert Vogt ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Angiotensin Receptor Blockers ◽  
Dietary Sodium ◽  
Angiotensin Receptor ◽  
High Potassium ◽  
Potassium Intake ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Urinary Potassium

Abstract Background Angiotensin receptor blockers (ARBs) lower blood pressure (BP) and proteinuria and reduce renal disease progression in many—but not all—patients. Reduction of dietary sodium intake improves these effects of ARBs. Dietary potassium intake affects BP and proteinuria. We set out to address the effect of potassium intake on BP and proteinuria response to losartan in non-diabetic proteinuric chronic kidney disease (CKD) patients. Methods We performed a post-hoc analysis of a placebo-controlled interventional cross-over study in 33 non-diabetic proteinuric patients (baseline mean arterial pressure and proteinuria: 105 mmHg and 3.8 g/d, respectively). Patients were treated for 6 weeks with placebo, losartan, and losartan/hydrochlorothiazide, combined with a habitual (∼200 mmol/d) and low-sodium diet (<100 mmol/d), in randomized order. To analyze the effects of potassium intake, we categorized patients based on median split of 24 h urinary potassium excretion, reflecting potassium intake. Results Mean potassium intake was stable during all 6 treatment periods. Losartan and losartan/hydrochlorothiazide lowered BP and proteinuria in all treatment groups. Patients with high potassium intake showed no difference in the BP effects compared to patients with low potassium intake. The antiproteinuric response to losartan monotherapy and losartan combined with hydrochlorothiazide during the habitual sodium diet was significantly diminished in patients with high potassium intake (20% vs. 41%, p = 0.011 and 48% vs 64%, p = 0.036). These differences in antiproteinuric response abolished when shifting to the low sodium diet. Conclusions In proteinuric CKD patients, the proteinuria, but not BP-lowering response to losartan during a habitual high sodium diet was hampered during high potassium intake. Differences disappeared after sodium status change by low-sodium diet.

scholarly journals Oxytocin response to controlled dietary sodium and angiotensin II among healthy individuals

2018 ◽  
Vol 315 (4) ◽  
pp. E671-E675 ◽  
Author(s):  
Suman Srinivasa ◽  
Anna Aulinas ◽  
Timothy O’Malley ◽  
Patrick Maehler ◽  
Gail K. Adler ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Healthy Individuals ◽  
Fasting Serum ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Before And After

Oxytocin, while classically known for its role in parturition, lactation, and social behavior, also has been implicated in the control of sodium homeostasis in animal models. To improve our understanding of oxytocin physiology in humans, we measured basal oxytocin levels under low- and liberal-dietary-sodium conditions and following a peripheral angiotensin II (ANG II) infusion. Ten healthy individuals underwent a 6-day standardized low-sodium diet and a 6-day liberal-sodium diet. Each diet was followed by a graded ANG II infusion for 30-min sequential intervals at doses of 0.3, 1.0, and 3.0 ng·kg−1·min−1. Fasting serum oxytocin was assessed before and after ANG II infusion. Basal oxytocin levels (1,498.5 ± 94.7 vs. 1,663.3 ± 213.9 pg/ml, P = 0.51) did not differ after the low- and liberal-sodium diets. Following the ANG II infusion, ANG II levels and mean arterial pressure significantly increased as expected. In contrast, the ANG II infusion significantly lowered oxytocin levels from 1,498.5 ± 94.7 vs. 1,151.7 ± 118.1 pg/ml ( P < 0.001) on the low-sodium diet and from 1,663.3 ± 213.9 vs. 1,095.2 ± 87.4 pg/ml ( P = 0.03) on the liberal-sodium diet. The percent change in oxytocin following the ANG II infusion did not differ by sodium diet (−25 ± 5% vs. −28 ± 7% low- vs. liberal-sodium conditions, P > 0.99). Dietary sodium intake did not affect circulating oxytocin levels among healthy individuals. Systemic oxytocin levels were significantly suppressed following a peripheral ANG II infusion independent of dietary sodium conditions.

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