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.

Contrasting endocrine responses to acute oral compared with intravenous sodium loading in normal humans

1998 ◽  
Vol 274 (1) ◽  
pp. F111-F119 ◽  
Author(s):  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Martin G. Buckley ◽  
Michelle A. Miller ◽  
Giuseppe A. Sagnella ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Fold Increase ◽  
Early Response ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Loading ◽  
Sodium Load ◽  
Intravenous Sodium ◽  
Oral Sodium

There is evidence in animals and in humans for accelerated natriuresis after oral compared with intravenous sodium loading. To assess the role of atrial natriuretic peptide (ANP) as a contributory mechanism, we compared the hormonal responses to an intravenous sodium load and to the same sodium load taken orally in three separate groups of healthy subjects in balance on low, normal, or high sodium intake. On each diet, there was a trend for an early delay in sodium excretion, followed by increased natriuresis after the oral compared with intravenous sodium load. On all levels of dietary sodium intake, there was a significant (∼2-fold) increase in plasma ANP levels after intravenous saline infusion. There was a significant suppression of the renin system both after oral and intravenous sodium loading. However, there was no acute increase in plasma ANP levels after the oral sodium load, except on the very low sodium intake. This striking and unexpected observation suggests that changes in plasma ANP levels appear to play little role in the early response to an acute oral sodium load in subjects with sodium intake in the range of 150–350 mmol/day. Endocrine mechanisms for the accelerated increase in sodium excretion after oral compared with intravenous sodium loading remain to be elucidated.

Gastrointestinal osmoreceptors and renal sodium excretion in humans

2000 ◽  
Vol 278 (2) ◽  
pp. R287-R294 ◽  
Author(s):  
Lars Juel Andersen ◽  
Thomas Ulrik Skram Jensen ◽  
Morten Heiberg Bestle ◽  
Peter Bie
Keyword(s):  
Hypertonic Saline ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Plasma Sodium ◽  
Salt Loading ◽  
Water Loading ◽  
Renal Sodium Excretion ◽  
Stimulation Of

The hypothesis that natriuresis can be induced by stimulation of gastrointestinal osmoreceptors was tested in eight supine subjects on constant sodium intake (150 mmol NaCl/day). A sodium load equivalent to the amount contained in 10% of measured extracellular volume was administered by a nasogastric tube as isotonic or hypertonic saline (850 mM). In additional experiments, salt loading was replaced by oral water loading (3.5% of total body water). Plasma sodium concentration increased after hypertonic saline (+3.1 ± 0.7 mM), decreased after water loading (−3.8 ± 0.8 mM), and remained unchanged after isotonic saline. Oncotic pressure decreased by 9.4 ± 1.2, 3.7 ± 1.2, and 10.7 ± 1.3%, respectively. Isotonic saline induced an increase in renal sodium excretion (104 ± 15 to 406 ± 39 μmol/min) that was larger than seen with hypertonic saline (85 ± 15 to 325 ± 39 μmol/min) and water loading (88 ± 11 to 304 ± 28 μmol/min). Plasma ANG II decreased to 22 ± 6, 35 ± 6, and 47 ± 5% of baseline after isotonic saline, hypertonic saline, and water loading, respectively. Plasma atrial natriuretic peptide (ANP) concentrations and urinary excretion rates of endothelin-1 were unchanged. In conclusion, stimulation of osmoreceptors by intragastric infusion of hypertonic saline is not an important natriuretic stimulus in sodium-replete subjects. The natriuresis after intragastric salt loading was independent of ANP but can be explained by inhibition of the renin-angiotensin system.

Natriuresis induced by mild hypernatremia in humans

2002 ◽  
Vol 282 (6) ◽  
pp. R1754-R1761 ◽  
Author(s):  
Lars Juel Andersen ◽  
Jens Lundbæk Andersen ◽  
Bettina Pump ◽  
Peter Bie
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Renal Sodium Excretion ◽  
Body Fluid Volume ◽  
Atrial Natriuretic

The hypothesis that increases in plasma sodium induce natriuresis independently of changes in body fluid volume was tested in six slightly dehydrated seated subjects on controlled sodium intake (150 mmol/day). NaCl (3.85 mmol/kg) was infused intravenously over 90 min as isotonic (Iso) or as hypertonic saline (Hyper, 855 mmol/l). After Hyper, plasma sodium increased by 3% (142.0 ± 0.6 to 146.2 ± 0.5 mmol/l). During Iso a small decrease occurred (142.3 ± 0.6 to 140.3 ± 0.7 mmol/l). Iso increased estimates of plasma volume significantly more than Hyper. However, renal sodium excretion increased significantly more with Hyper (291 ± 25 vs. 199 ± 24 μmol/min). This excess was not mediated by arterial pressure, which actually decreased slightly. Creatinine clearance did not change measurably. Plasma renin activity, ANG II, and aldosterone decreased very similarly in Iso and Hyper. Plasma atrial natriuretic peptide remained unchanged, whereas plasma vasopressin increased with Hyper (1.4 ± 0.4 to 3.1 ± 0.5 pg/ml) and decreased (1.3 ± 0.4 to 0.6 ± 0.1 pg/ml) after Iso. In conclusion, the natriuretic response to Hyper was 50% larger than to Iso, indicating that renal sodium excretion may be determined partly by plasma sodium concentration. The mechanism is uncertain but appears independent of changes in blood pressure, glomerular filtration rate, the renin system, and atrial natriuretic peptide.

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.

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.

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.

Time-course and relationship of the early changes in renal sodium excretion and aldosterone secretion during dietary sodium restriction in normal man

1990 ◽  
Vol 78 (6) ◽  
pp. 605-612 ◽  
Author(s):  
D. J. S. Carmichael ◽  
M. S. Sutters ◽  
R. J. Unwin ◽  
D. Gordon ◽  
J. Few ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Low Sodium ◽  
Renal Sodium Excretion ◽  
Plasma Arginine

1. The fall in renal sodium excretion after dietary sodium restriction is prompt and reproducible. The importance of increased aldosterone secretion during the early phase (within 48 h) of this response is unclear. Using two indirect measures of aldosterone secretion (in urine and saliva), we have tried to relate changes in excretion and concentration of this hormone to renal sodium excretion during the abrupt transition from a normal (approximately 150 mmol/day) or high (260 mmol/day) to a low (5–25 mmol/day) sodium intake in 11 and seven male volunteers, respectively. 2. All subjects showed reduced renal sodium excretion within 36 h of dietary restriction, but the times at which increases in renal aldosterone excretion, saliva aldosterone concentration and plasma renin activity became statistically significant varied widely (8–72 h, 2.5–>62.5 h and 38 h for renal aldosterone secretion, saliva aldosterone concentration and plasma renin activity, respectively). Circadian fluctuations in saliva aldosterone concentration were apparent and increased in amplitude during sodium restriction. 3. Urine flow rate tended to increase on the first day of sodium restriction and this reached statistical significance in the group initially on a high sodium intake (64.0 ± 8.8 to 84.3 ± 11.2 ml/h, P <0.01); although the pattern of urine flow did correlate with plasma arginine vasopressin concentration (r = −0.49, P <0.01), there was no significant decrease in mean plasma arginine vasopressin concentration [1.15 (0.92–1.44) to 0.90 (0.72–1.12) pmol/l, P = 0.08; geometric mean and 95% confidence limits]. Renal arginine vasopressin excretion fell significantly after the change from a normal or high to a low sodium diet [2.70 (2.38–8.69) to 2.19 (1.72–4.00) and 3.80 (2.92–5.01) to 2.50 (1.26–2.35) pmol/h, respectively, P <0.05]; in four subjects assayed, plasma atrial natriuretic peptide concentration also fell significantly [20.1 (16.3–24.9)to 13.1 (10.6–16.2) pmol/l, P <0.05]. 4. We conclude that after acute dietary sodium withdrawal: (1) unless enhanced renal sensitivity to aldosterone develops rapidly, increased secretion alone is unlikely to account for the initial decline in renal sodium excretion; (2) decreased atrial natriuretic peptide secretion may have a permissive role in ‘low-sodium’ adaptation; (3) the early ‘low-sodium’ diuresis is probably vasopressin-dependent and is an important mechanism in the preservation of normal plasma osmolality.

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.

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