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Gastrointestinal osmoreceptors and renal sodium excretion in humans

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@article{38363d2c98ab4b648e5d84a5b88b9ce5,
title = "Gastrointestinal osmoreceptors and renal sodium excretion in humans",
abstract = "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 micromol/min) that was larger than seen with hypertonic saline (85 +/- 15 to 325 +/- 39 micromol/min) and water loading (88 +/- 11 to 304 +/- 28 micromol/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.",
keywords = "Adult, Angiotensin II, Atrial Natriuretic Factor, Digestive System Physiological Phenomena, Drinking, Endothelin-1, Humans, Intubation, Gastrointestinal, Isotonic Solutions, Kidney, Male, Saline Solution, Hypertonic, Sodium, Sodium Chloride, Water-Electrolyte Balance",
author = "Andersen, {L J} and Skram, {Thomas Ulrik} and Bestle, {M H} and P Bie",
year = "2000",
month = "2",
language = "English",
volume = "278",
pages = "R287--94",
journal = "American Journal of Physiology: Regulatory, Integrative and Comparative Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Gastrointestinal osmoreceptors and renal sodium excretion in humans

AU - Andersen, L J

AU - Skram, Thomas Ulrik

AU - Bestle, M H

AU - Bie, P

PY - 2000/2

Y1 - 2000/2

N2 - 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 micromol/min) that was larger than seen with hypertonic saline (85 +/- 15 to 325 +/- 39 micromol/min) and water loading (88 +/- 11 to 304 +/- 28 micromol/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.

AB - 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 micromol/min) that was larger than seen with hypertonic saline (85 +/- 15 to 325 +/- 39 micromol/min) and water loading (88 +/- 11 to 304 +/- 28 micromol/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.

KW - Adult

KW - Angiotensin II

KW - Atrial Natriuretic Factor

KW - Digestive System Physiological Phenomena

KW - Drinking

KW - Endothelin-1

KW - Humans

KW - Intubation, Gastrointestinal

KW - Isotonic Solutions

KW - Kidney

KW - Male

KW - Saline Solution, Hypertonic

KW - Sodium

KW - Sodium Chloride

KW - Water-Electrolyte Balance

M3 - Journal article

VL - 278

SP - R287-94

JO - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

JF - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

SN - 0363-6119

IS - 2

ER -

ID: 44512315