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.

Acute renal denervation produces a diuresis and natriuresis in young SHR but not WKY rats

1986 ◽  
Vol 251 (4) ◽  
pp. F655-F661 ◽  
Author(s):  
M. A. Rudd ◽  
R. S. Grippo ◽  
W. J. Arendshorst
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Strain Differences ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Clearance experiments were conducted to determine the effect of acute unilateral renal denervation (DNX) on renal hemodynamics and salt and water excretion in anesthetized 6-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto genetic control rats (WKY). Before DNX, SHR had higher mean arterial pressure (33%) and renal vascular resistance (RVR) (57%) and lower glomerular filtration rate (GFR) (10%); urine flow and sodium excretion were similar. Following DNX in SHR, sodium and water excretion increased by 138 and 62%, respectively (P less than 0.001); GFR and RVR were unchanged. In contrast, DNX in WKY did not affect urine flow (0%) or sodium excretion (-21%). These strain differences were observed in Okamoto-Aoki rats from two sources. Effective DNX was indicated by 95% reduction of norepinephrine content 3 days after DNX in both strains. Six-week-old Sprague-Dawley and Munich-Wistar rats, in contrast to WKY, responded to DNX with a natriuresis (+182%) and diuresis (+95%) (P less than 0.001). Renal function was unaffected by sham DNX in SHR. Our results indicate that efferent renal nerve activity has little tonic influence on the renal vasculature in these young rats. Augmented neurotransmitter release and/or tubular responsiveness may be involved in fluid and electrolyte retention and the pathogenesis of hypertension in SHR. Conversely, blunted renal neuroeffector responses may prevent WKY from developing hypertension.

Sodium chloride preference of genetically hypertensive and normotensive rats

1983 ◽  
Vol 245 (1) ◽  
pp. R38-R44 ◽  
Author(s):  
R. Di Nicolantonio ◽  
F. A. Mendelsohn ◽  
J. S. Hutchinson
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Sodium Intake ◽  
Bb Rat ◽  
Dark Agouti ◽  
Sprague Dawley ◽  
Saline Preference ◽  
Wistar Kyoto ◽  
Preference Tests ◽  
Genetically Hypertensive

Preference for 0.9% saline was examined, using two-bottle preference tests over 6-7 days, in the spontaneously hypertensive rat (SHR) and normotensive Wistar Kyoto rat (WK) of the Okamoto strain, the genetically hypertensive (GHR) and normotensive rat (NT) of the Smirk strain, and the Sprague-Dawley (SD), Dark Agouti (DA), and hooded Long-Evans or Brattleboro (BB) rat. Only the SHR exhibited a sustained and marked preference for 0.9% saline on each test day. The WK, GHR, NT, and SD preferred saline in the first 24-48 h of testing but thereafter showed neither a preference for, nor aversion to, saline. The BB showed neither a preference for, nor aversion to, saline in the first 24 h of testing and thereafter showed a significant aversion to saline on each test day. Saline preference was further examined in both the SHR and WK offered a choice of water and 0.9%, 2.0, or 2.7% saline. While preference for saline decreased in both SHR and WK with increasing saline concentration, the SHR maintained a significantly greater preference for saline and greater total sodium intake than the WK at each concentration. Hydralazine (5 mg . kg-1 . day-1, po) administered to SHR, while they were offered a choice of water and 0.9% saline, significantly lowered blood pressure over a 4-day period but failed to alter their saline preference significantly. We conclude that of the seven strains of rats examined only the SHR exhibited a preference for saline in extended two-bottle preference tests. Furthermore this preference for saline appears to be maintained independently of the blood pressure of the SHR.

Feeding-induced increase in urinary dopamine excretion is independent of renal innervation and sodium intake

1994 ◽  
Vol 266 (4) ◽  
pp. F563-F567
Author(s):  
B. Muhlbauer ◽  
H. Osswald
Keyword(s):  
Time Course ◽  
Sodium Intake ◽  
Tap Water ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Urinary Dopamine ◽  
Renal Innervation

Food intake increases urinary dopamine excretion. To investigate the role of renal nerve activity in this renal response to feeding, we studied urinary dopamine excretion after chronic bilateral renal denervation (DNX, n = 8) in male Sprague-Dawley rats. Controls were sham operated (CON, n = 6). In a paired crossover design, animals were studied both in fed and fasted state. Time course measurements of renal tissue norepinephrine (NE) content in a third group of DNX rats showed a decrease by 90% not earlier than 18 h post-DNX, remaining to be reduced to this level until day 11. Renal NE content in DNX animals was measured at the end of the study to confirm complete denervation. In 24-h urine, collected from fed and fasted conscious CON and DNX rats in metabolic cages, concentrations of dopamine and sodium were measured during two different sodium intake regimens, i.e., tap water and 1 g/dl NaCl as drinking water. No influence of renal innervation on urinary dopamine could be observed in fed and fasted animals. The marked changes in urinary volume and sodium output due to the different sodium regimens were not paralleled by urinary dopamine excretion. However, urinary dopamine was increased 2.1- to 2.4-fold (P < 0.01) because of feeding in all groups, independent of sodium balance and renal innervation. We conclude that in conscious rats both basal urinary dopamine excretion and its marked increase in response to feeding are independent of sodium balance and of renal nerve activity.

Osmoregulatory control of renal sodium excretion after sodium loading in humans

1998 ◽  
Vol 275 (6) ◽  
pp. R1833-R1842 ◽  
Author(s):  
Lars Juel Andersen ◽  
Peter Norsk ◽  
Lars Bo Johansen ◽  
Poul Christensen ◽  
Thomas Engstrøm ◽  
...  
Keyword(s):  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Venous Pressure ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Central Venous ◽  
Salt Loading ◽  
Significant Difference

The hypothesis that renal sodium handling is controlled by changes in plasma sodium concentration was tested in seated volunteers. A standard salt load (3.08 mmol/kg body wt over 120 min) was administered as 0.9% saline (Isot) or as 5% saline (Hypr) after 4 days of constant sodium intake of 75 (LoNa+) or 300 mmol/day (HiNa+). Hypr increased plasma sodium by ∼4 mmol/l but increased plasma volume and central venous pressure significantly less than Isot irrespective of diet. After LoNa+, Hypr induced a smaller increase in sodium excretion than Isot (48 ± 8 vs. 110 ± 17 μmol/min). However, after HiNa+the corresponding natriureses were identical (135 ± 33 vs. 139 ± 39 μmol/min), despite significant difference between the increases in central venous pressure. Decreases in plasma ANG II concentrations of 23–52% were inversely related to sodium excretion. Mean arterial pressure, plasma oxytocin and atrial natriuretic peptide concentrations, and urinary excretion rates of endothelin-1 and urodilatin remained unchanged. The results indicate that an increase in plasma sodium may contribute to the natriuresis of salt loading when salt intake is high, supporting the hypothesis that osmostimulated natriuresis is dependent on sodium balance in normal seated humans.

Role of sodium and water excretion in the antihypertensive effect of vasopressin in the spontaneously hypertensive rat

1992 ◽  
Vol 70 (10) ◽  
pp. 1309-1314 ◽  
Author(s):  
E. K. Y. Chiu ◽  
H. Wang ◽  
J. R. McNeill
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rat ◽  
Control Level ◽  
Sprague Dawley ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Vasopressin Infusion ◽  
Hypertensive Rat ◽  
Wistar Kyoto

Mean arterial pressure (mmHg (1 mmHg = 133.322 Pa)), sodium excretion rate (μmol∙kg−1∙min−1), and urine flow (μL∙kg−1∙min−1) were measured in conscious unrestrained spontaneously hyptertensive rats (SHR) and normotensive Wistar–Kyoto rats (WKY) before, during, and after a 3-h intravenous infusion of arginine vasopressin (20 ng∙kg−1∙min−1), an equipressor dose of phenylephrine, or an infusion of the vehicle. Cessation of the phenylephrine infusion was associated with a return of arterial pressure to preinfusion control values in both SHR and WKY. Cessation of the vasopressin infusion was also associated with a return of arterial pressure to preinfusion values in WKY. In contrast, in the SHR, arterial pressure fell from a preinfusion control level of 164 ± 6.2 to 137 ± 4 mmHg within 1 h of stopping the vasopressin infusion. Five hours after stopping the infusion, pressure was 134 ± 3 mmHg (29 ± 5 mmHg below preinfusion levels). Similar to the WKY, cessation of a vasopressin infusion was associated with a return of arterial pressure to preinfusion values in Sprague–Dawley rats. Thus, the failure to observe a hypotensive response in normotensive rats was not a peculiarity of the WKY strain. Sodium excretion rates increased during the infusions of vasopressin to a greater extent in SHR than in WKY. However, the natriuresis induced by phenylephrine was not significantly different from that generated by vasopressin in SHR, and in WKY, the natriuresis was greater for phenylephrine than for vasopressin. Urine output increased to a greater extent during the infusions of phenylephrine in both SHR and WKY than during vasopressin infusion. Because the infusions of phenylephrine were associated with either a similar or greater natriuresis and diuresis than the infusions of vasopressin, it is unlikely that the large fall in arterial pressure that occurred following the withdrawal of the vasopressin infusion (the "withdrawal-induced antihypertensive phenomenon") was related to the preceding natriuresis and diuresis.Key words: vasopressin, spontaneously hypertensive rat, sodium excretion, water excretion, renal function, phenylephrine.

Dietary Sodium Intake: A Determinant of Postprandial Plasma Sodium Concentration in the Dog

1982 ◽  
Vol 62 (5) ◽  
pp. 471-477 ◽  
Author(s):  
E. G. Schneider ◽  
Sarah D. Gleason ◽  
A. Zucker
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Free Access ◽  
Potassium Excretion ◽  
Plasma Sodium Concentration

1. The effect of dietary sodium intake on pre-and post-prandial plasma sodium concentrations and on the pattern of sodium and potassium excretion was determined in conscious female dogs, who were allowed free access to water and were fed on commercial low sodium diets supplemented with 0, 50, 100 or 250 mmol of sodium chloride/day for 6 days. 2. The preprandial plasma sodium concentration was not altered by the dietary sodium intake. However, the 4 h postprandial plasma sodium concentration was linearly related to the magnitude of dietary sodium intake, whereas the 8 h postprandial plasma sodium concentration was elevated only in dogs receiving 250 mmol of sodium/day. 3. The (0–8 h/0–24 h) ratio for urinary sodium excretion was significantly correlated with both the dietary sodium intake and the postprandial increase in plasma sodium concentration. 4. The 24 h excretion of potassium was not markedly affected by the dietary sodium intake; however, the (0–8 h/0–24 h) ratio for potassium excretion was significantly correlated with both the dietary sodium intake and the (0–8 h/0–24 h) ratio for sodium excretion. 5. These data indicate that: (a) postprandial increases in plasma sodium concentration need to be considered when evaluating the mechanisms involved in the daily regulation of sodium balance; (b) the daily pattern of potassium excretion is closely linked to the dietary sodium intake.

Evidence that intrarenal bradykinin plays a role in regulation of renal function

1993 ◽  
Vol 265 (4) ◽  
pp. E648-E654 ◽  
Author(s):  
H. M. Siragy
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Kinin System ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium

Bradykinin (BK) is produced by the kidney, but the role of the renal kallikrein-kinin system (KKS) in the control of renal function is not understood. We studied the effects of intrarenal infusion of the BK antagonist, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-trifluoroacetic acid (BKA, n = 5) and BK (n = 4) alone or combined with antagonist (BKA 0.025 ng.kg-1 x min-1 + BK 0.25 ng.kg-1 x min-1, n = 4) in uninephrectomized conscious dogs in sodium balance at 10 and 80 meq/day. During low sodium intake, administration of BKA (infusions from 0.025 to 2.5 ng.kg-1 x min-1) caused a significant antidiuresis (P < 0.0001) and antinatriuresis (P < 0.0001) and a decrease in fractional sodium excretion (P < 0.0001). There were no changes in estimated renal plasma flow (RPF) or glomerular filtration rate during intrarenal administration of BKA at 0.025 and 0.25 ng.kg-1 x min-1. A dose of 2.5 ng.kg-1 x min-1 BKA caused a significant decrease in RPF. There were no changes in plasma aldosterone concentration, plasma renin activity, or systemic arterial pressure during intrarenal BKA administration. At 80 meq/day sodium balance (n = 5), intrarenal administration of BKA did not cause any systemic or renal effects. Intrarenal administration of BK at 0.25 ng.kg-1 x min-1 during low sodium balance caused an increase in urine flow rate and urinary sodium excretion. Coinfusion of BK with BKA completely abrogated the renal excretory changes induced by BKA. These data suggest that intrarenal KKS plays a role in control of renal function largely by a tubular mechanism during low sodium intake.

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

Role of endogenous central opioid mechanisms in maintenance of body sodium balance

1995 ◽  
Vol 268 (3) ◽  
pp. R723-R730 ◽  
Author(s):  
D. R. Kapusta ◽  
J. C. Obih
Keyword(s):  
Sodium Intake ◽  
Dietary Sodium ◽  
Opioid Antagonist ◽  
Sodium Balance ◽  
Sodium Restriction ◽  
Sprague Dawley ◽  
Intracerebroventricular Infusion ◽  
Sprague Dawley Rats ◽  
Body Sodium

The role of endogenous central opioids in the regulation of renal function was studied in Sprague-Dawley rats. In metabolism studies, changes in sodium balance were examined during normal dietary sodium intake (days 1-7; Na+ of 174 meq/kg) and sodium restriction (days 8-14; Na+ of 4.0 meq/kg). The influence of endogenous central opioids was investigated by repeating the protocol in the same rats during intracerebroventricular infusion of the opioid antagonist naltrexone methylbromide (NMBR). Intracerebroventricular NMBR did not alter sodium balance in rats fed normal sodium chow. In contrast, on low-sodium days 8 and 9, rats exhibited a more negative sodium balance during intracerebroventricular NMBR (day 8; -1,191 +/- 37 mu eq) compared with respective predrug control levels (day 8; -641 +/- 39 mu eq). Subcutaneous NMBR did not alter renal adaptation to sodium restriction. Thus central opioids are not involved in the maintenance of sodium balance during normal sodium intake. However, when dietary sodium is restricted, central opioid pathways are activated as a mechanism to maximally retain sodium.

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.

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