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1 Department of Medical Physiology, Panum Institute, University of Copenhagen, and 2 Danish Aerospace Medical Centre of Research, Rigshospitalet, DK-2200 Copenhagen; 3 Department of Clinical Physiology, Herlev Hospital, DK-2730 Herlev; and 4 Department of Physiology and Pharmacology, University of Southern Denmark, Odense, DK-5000 Odense, Denmark
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.
hypertonic saline; isotonic saline; angiotensin II; atrial natriuretic peptide; endothelin-1
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