scholarly journals Mechanisms of sodium balance: total body sodium, surrogate variables, and renal sodium excretion

2018 ◽  
Vol 315 (5) ◽  
pp. R945-R962 ◽  
Author(s):  
Peter Bie
Keyword(s):  
Steady State ◽  
Sodium Excretion ◽  
Sodium Balance ◽  
Sodium Homeostasis ◽  
Renal Sodium Excretion ◽  
Body Sodium ◽  
Surrogate Variables ◽  
Total Body ◽  
Pressure Natriuresis

The classical concepts of human sodium balance include 1) a total pool of Na+ of ≈4,200 mmol (total body sodium, TBS) distributed primarily in the extracellular fluid (ECV) and bone, 2) intake variations of 0.03 to ≈6 mmol·kg body mass−1·day−1, 3) asymptotic transitions between steady states with a halftime (T½) of 21 h, 4) changes in TBS driven by sodium intake measuring ≈1.3 day [ΔTBS/Δ(Na+ intake/day)], 5) adjustment of Na+ excretion to match any diet thus providing metabolic steady state, and 6) regulation of TBS via controlled excretion (90–95% renal) mediated by surrogate variables. The present focus areas include 1) uneven, nonosmotic distribution of increments in TBS primarily in “skin,” 2) long-term instability of TBS during constant Na+ intake, and 3) physiological regulation of renal Na+ excretion primarily by neurohumoral mechanisms dependent on ECV rather than arterial pressure. Under physiological conditions 1) the nonosmotic distribution of Na+ seems conceptually important, but quantitatively ill defined; 2) long-term variations in TBS represent significant deviations from steady state, but the importance is undetermined; and 3) the neurohumoral mechanisms of sodium homeostasis competing with pressure natriuresis are essential for systematic analysis of short-term and long-term regulation of TBS. Sodium homeostasis and blood pressure regulation are intimately related. Real progress is slow and will accelerate only through recognition of the present level of ignorance. Nonosmotic distribution of sodium, pressure natriuresis, and volume-mediated regulation of renal sodium excretion are essential intertwined concepts in need of clear definitions, conscious models, and future attention.

Sodium homeostasis in conscious dogs after chronic cardiac denervation

1990 ◽  
Vol 258 (4) ◽  
pp. F805-F811 ◽  
Author(s):  
G. Kaczmarczyk ◽  
E. Schmidt
Keyword(s):  
Sodium Excretion ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Right Atrial ◽  
Sodium Balance ◽  
Cardiac Denervation ◽  
Arterial Blood ◽  
Renal Sodium Excretion ◽  
Body Sodium ◽  
Total Body

The ability to regulate renal sodium excretion after an acute reduction of total body sodium by peritoneal dialysis (PD) and subsequent dietary sodium repletion was investigated in 12 [6 intact, 6 chronically cardiac denervated (CD)] conscious, chronically instrumented dogs. For 10 days, balance experiments were performed with daily measurements of mean arterial blood pressure (MABP), right atrial pressure (RAP), and heart rate (HR). The prepared diet contained 0.5 (days 1-3 after PD) or 2.5 mmol Na.kg body wt-1.day-1 (control day and days 4-9 after PD). Control values were all similar in both groups except higher fasting plasma renin activities (PRA) were observed in the CD dogs [2.6 +/- 0.4 vs. 1.0 +/- 0.2 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.05]. Days 1-4 after PD, RAP fell in both groups by 2-3 cmH2O, and renal sodium excretion decreased abruptly. PRA increased to 22.8 +/- 4.1 (intact) and 29.9 +/- 4.9 ng ANG I.ml-1.h-1 (CD dogs) (day 3 after PD). Both groups continued to retain sodium, and when it was available again, PRA decreased. After the amount of sodium lost by PD was regained, the intact dogs remained in a balanced equilibrium. In the CD dogs, PRA was still above control, and they retained sodium in excess (+ 1.9 +/- 0.1 mmol/kg body wt). We conclude that the cardiac nerves are not essential for stimulating PRA and sodium retention after an acute sodium deficit. However, the inhibition of PRA and the rapid adjustment of sodium balance during sodium repletion is impaired after cardiac denervation.

scholarly journals Total Body Sodium Balance in Chronic Kidney Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Kylie Martin ◽  
Sven-Jean Tan ◽  
Nigel D. Toussaint
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Sodium Intake ◽  
Dynamic Assessment ◽  
Sodium Balance ◽  
Sodium Homeostasis ◽  
Body Sodium ◽  
Clinical Associations ◽  
Total Body ◽  
Tissue Sodium

Excess sodium intake is a leading but modifiable risk factor for mortality, with implications on hypertension, inflammation, cardiovascular disease, and chronic kidney disease (CKD). This review will focus mainly on the limitations of current measurement methods of sodium balance particularly in patients with CKD who have complex sodium physiology. The suboptimal accuracy of sodium intake and excretion measurement is seemingly more marked with the evolving understanding of tissue (skin and muscle) sodium. Tissue sodium represents an extrarenal influence on sodium homeostasis with demonstrated clinical associations of hypertension and inflammation. Measurement of tissue sodium has been largely unexplored in patients with CKD. Development and adoption of more comprehensive and dynamic assessment of body sodium balance is needed to better understand sodium physiology in the human body and explore therapeutic strategies to improve the clinical outcomes in the CKD population.

Contribution of pressure natriuresis to control of total body sodium: balance studies in freely moving dogs

2001 ◽  
Vol 537 (3) ◽  
pp. 941-947 ◽  
Author(s):  
E. Seeliger ◽  
E. Safak ◽  
P. B Persson ◽  
H W. Reinhardt
Keyword(s):  
Sodium Balance ◽  
Body Sodium ◽  
Freely Moving ◽  
Total Body ◽  
Pressure Natriuresis

Sodium regulation in the larvae of Chironomus dorsalis (Meig.) and Camptochironomus tentans (Fabr.): the effect of slat depletion and some observations on temperature changes

1975 ◽  
Vol 62 (1) ◽  
pp. 121-139
Author(s):  
DA Wright
Keyword(s):  
Surrounding Medium ◽  
The Body ◽  
Sodium Balance ◽  
Primary Role ◽  
Secondary Importance ◽  
Temperature Changes ◽  
Body Sodium ◽  
Total Body ◽  
Sodium Regulation ◽  
Anal Papillae

Sodium regulation was studied in fourth instar larvae of Chironomus dorsalis and Camptochironomus tentans. Both maintain a body sodium level well above that of the surrounding medium. The haemolymph contains approximately 90% of total body sodium and approximates to a single compartment freely exchanging sodium with the external medium. The anal papillae play a primary role in sodium regulation, the gut being in secondary importance. Sodium regulation in both species is comparatively insensitive to alterations in acclimatization temperature. C. dorsalis and C. tentans are capable of maintaining sodium balance in media containing 10 mumole Na and 25 mumole Na respectively. When exposed to several changes of distilled water, C. tentansis capable of reducing sodium loss by elaboration of a more dilute urine. This is apparently,supplemented by a reduction in the permeability of the body surface. Activation of sodium uptake in both species is comparatively sluggish, with influx reaching a maximum only after the loss of greater than 30% body sodium.

scholarly journals Renin Inhibition Improves Pressure Natriuresis in Essential Hypertension

2000 ◽  
Vol 11 (10) ◽  
pp. 1813-1818
Author(s):  
PIETER VAN PAASSEN ◽  
DICK DE ZEEUW ◽  
PAUL E. DE JONG ◽  
GERJAN NAVIS
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Raas Blockade ◽  
Renin Inhibition ◽  
Pressure Natriuresis

Abstract. Pressure natriuresis (PN), i.e., a rise in renal sodium excretion in response to a higher BP, is involved in long-term BP regulation. PN is blunted in essential hypertension, but the mechanism is unknown. This study assessed the role of the renin-angiotensin-aldosterone system (RAAS) in PN in eight essential hypertensive men from the individual correlations between spontaneous fluctuations in BP and time corresponding changes in sodium excretion (collected at 2- and 4-h intervals for 48 h), during strict sodium balance, without treatment, and during renin inhibition (remikiren, 600 mg oral compound). Without treatment, daily values for mean arterial pressure were 109.5 ± 1.9 and 107 ± 1.9 mmHg, for urinary sodium excretion were 37.2 ± 2.8 and 42.0 ± 2.8 mmol/24 h, and for plasma renin activity were 2.34 ± 0.48 and 2.23 ± 0.44 nmol/L per h, respectively, for two consecutive days. During remikiren treatment, mean arterial pressure was 101.9 ± 1.7 and 100.8 ± 1.7 mmHg (P < 0.05, versus baseline). Urinary sodium excretion was 39.3 ± 3.7 and 45.2 ± 5.3 mmol/24 h (not significant versus baseline), and plasma renin activity was 0.79 ± 0.11 and 0.82 ± 0.13 nmol/L per h (P < 0.05 versus baseline). During remikiren treatment, BP correlated positively with sodium excretion in all patients but in only three of eight patients without treatment. The slope of the regression equation was steeper during remikiren treatment in seven of eight patients. Thus, the relationship between BP and natriuresis was more readily apparent during RAAS blockade, suggesting that RAAS activity blunts PN in hypertensive patients. Improved PN may contribute to the hypotensive effect of RAAS blockade and to maintenance of sodium balance at a lower BP level without volume expansion.

scholarly journals Low-Dose Nitric Oxide Inhibition Produces a Negative Sodium Balance in Conscious Dogs

2001 ◽  
Vol 12 (6) ◽  
pp. 1128-1136
Author(s):  
ERDMANN SEELIGER ◽  
PONTUS B. PERSSON ◽  
WILLEHAD BOEMKE ◽  
GÖTZ MOLLENHAUER ◽  
BENNO NAFZ ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Time Course ◽  
Low Dose ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Pressure Effects ◽  
Sodium Balance ◽  
Body Sodium ◽  
Natriuretic Effect ◽  
Total Body

Abstract. Nitric oxide modulates renal hemodynamics and salt and water handling. Studies on the latter have provided conflicting results, however. Electrolyte and water balances were therefore studied in 28 beagles for 4 d, to determine the various effects of nitric oxide synthase (NOS) inhibition on renal function. The dogs were chronically equipped with aortic occluders to reduce renal perfusion pressure (RPP), bladder catheters, and catheters for measurements of RPP and mean arterial BP. A swivel system allowed free movement within the kennels. In a first set of experiments, a nonpressor dose of L-Nω-nitroarginine (LN) (3 μg/min per kg body wt) was administered, to prevent increases in mean arterial BP and thus pressure effects on renin release and natriuresis. Remarkably, the nonpressor dose of LN caused a negative sodium balance. The natriuretic effect may involve reduced plasma renin activity, reduced aldosterone concentrations, and increased atrial natriuretic peptide concentrations. Changes in aldosterone levels, however, were the only parameters to parallel the time course of sodium excretion. In a second set of experiments, a sodium-retaining challenge was elicited by reduction of RPP. Dogs without NOS inhibition escaped sodium retention during RPP reduction after 2 d (“pressure escape”). LN neither ameliorated nor aggravated the sodium-retaining effect of reduced RPP, nor did it compromise the accomplishment of pressure escape. In conclusion, inhibition of NOS with a low dose of LN results in a reduction of total-body sodium. This effect mainly relies on reduced aldosterone concentrations. Furthermore, LN does not change the regulatory response to long-term RPP reduction.

scholarly journals Urodilatin, a kidney-derived natriuretic factor, is excreted with a circadian rhythm and is stimulated by saline infusion in man.

1991 ◽  
Vol 1 (9) ◽  
pp. 1109-1113
Author(s):  
C Drummer ◽  
F Fiedler ◽  
A König ◽  
R Gerzer
Keyword(s):  
Circadian Rhythm ◽  
Sodium Excretion ◽  
Isotonic Saline ◽  
Physiological Role ◽  
Urinary Sodium Excretion ◽  
Saline Infusion ◽  
Sodium Homeostasis ◽  
Peptide Family ◽  
Physiological Regulator

Urodilatin is a recently described, presumably kidney-derived member of the atrial natriuretic peptide family. The first data on a physiological role for urodilatin in the regulation of sodium homeostasis in humans is presented in this work. Urinary urodilatin excretion during a 9-day study in healthy volunteers paralleled the circadian rhythm in urinary sodium excretion. Furthermore, urodilatin and sodium excretion were slightly increased during the first 3 h after an acute isotonic saline infusion and about three-fold elevated during 14 h postinfusion; both parameters remained closely correlated up to 28 h postinfusion. These data suggest that urodilatin is involved in the circadian regulation of sodium excretion and is a physiological regulator of long-term sodium excretion after an acute saline infusion.

scholarly journals Natriuretic effect of 2 weeks of dapagliflozin treatment in patients with type 2 diabetes and preserved kidney function: results of the DAPASALT trial

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R Scholtes ◽  
M.H.A Muskiet ◽  
M.J.B Van Baar ◽  
P.J Greasley ◽  
C Karlsson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Steady State ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Funding Source ◽  
Treatment Change ◽  
Glucose Excretion

Abstract Background Sodium glucose co-transporter 2 (SGLT2) inhibitors reduce the risk for heart failure hospitalization, potentially by inducing sodium excretion, osmotic diuresis and plasma volume contraction, leading to more favorable systemic hemodynamic function. However, this hypothesis has never been formally investigated as no studies have assessed cumulative sodium excretion with SGLT2 inhibition during standardized sodium intake. Methods We conducted a mechanistic open label study in patients with type 2 diabetes mellitus (T2D) with preserved kidney function, who were receiving a standardized sodium intake (150 mmol/day) to evaluate the acute effects (average day 2–4), effects at steady state (average day 12–14) and effects during three days wash-out of dapagliflozin on sodium balance and blood pressure. Primary outcome measure was 24-hr sodium excretion during the acute phase. Secondary outcomes included 24-hr glucose excretion and 24-hr blood pressure at each time period and sodium excretion at steady state and during follow-up. Results Seventeen patients with T2D were enrolled (64.7% male, mean ± SD age 64.24±7.33 years, weight 99.54±17.36 kg, eGFR 94.53±10.10 mL/min/1.73m2, HbA1c 7.20±0.63%). Average sodium excretion at baseline was 147±32 mmol/24 hr, which did not significantly change during treatment (Change at day 2–4 [95% CI]: −5.21 [19.54, 9.12] mmol/24 hr; Change at Day 12–14 [95% CI]: 3.69 [−24.82, 32.20] mmol/24 hr). However, sodium excretion was reduced following washout compared to end of treatment (Change at Day 15–17 [95% CI]: −16.72 [−34.11, 0.66] mmol/24 hr). Glucose excretion was significantly increased throughout the study. Systolic blood pressure was 127.0±10.3 mmHg at baseline and significantly reduced at Day 3 [95% CI]: −5.27 [−8.55, −1.99] mmHg and Day 14 [95% CI]: −7.10 [−10.04, −4.16] mmHg compared to baseline and remained lower following washout. Conclusions This study shows that, during a standardized sodium intake, the SGLT-2 inhibitor dapagliflozin acutely reduces blood pressure without altering sodium excretion, indicating possible direct vascular effects independent of sodium balance. Funding Acknowledgement Type of funding source: Other. Main funding source(s): Astra Zeneca

Kinetics of sodium homeostasis in rats: rapid excretion and equilibration rates

1988 ◽  
Vol 254 (6) ◽  
pp. R1001-R1006 ◽  
Author(s):  
E. J. Holtzman ◽  
L. M. Braley ◽  
G. H. Williams ◽  
N. K. Hollenberg
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Hormonal Changes ◽  
Sprague Dawley ◽  
Sodium Homeostasis ◽  
Nocturnal Feeding ◽  
Normal Rat ◽  
Normal Humans ◽  
Wistar Kyoto

In normal humans, when sodium intake is abruptly reduced from a high to a very low level, renal sodium excretion falls exponentially (half time approximately 24 h), and several days are required to achieve external sodium balance, where intake equals excretion. Because much of our knowledge of intrarenal mechanisms comes from the rat, we studied their capacity to handle sodium. In two strains of rat, Sprague-Dawley (SD) and Wistar-Kyoto (WKY), whether the sodium load was administered intravenously, by gavage, or by spontaneous feeding, the slope relating sodium excretion to time was 8-10 times more rapid than in humans, reflecting half times of 2-3 h, and external sodium balance was achieved in hours rather than days. The combination of normal rat nocturnal feeding patterns and the rapidity of the response result in a daily spontaneous transition from an expanded state with a high or intermediate level of sodium excretion to a more contracted state, with minimal sodium excretion. Studies designed to assess sodium homeostasis in rats, and related renal and hormonal changes, must consider these rapid transitions, which are related, perhaps, to the rats' persistent and remarkably rapid growth.

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