Gastrointestinal osmoreceptors and renal sodium excretion in humans Andersen, Lars Juel; Jensen, Thomas Ulrik Skram; Bestle, Morten Heiberg ...
American journal of physiology. Regulatory, integrative and comparative physiology,
02/2000, Letnik:
278, Številka:
2
Journal Article
Recenzirano
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
Background
Neutrophil gelatinase associated lipocalin (NGAL) is proposed as a biomarker of acute kidney injury (AKI). NGAL has been studied in a range of body fluids including serum and EDTA plasma. ...The aim of the present study was to establish relationship between serum NGAL concentrations and EDTA plasma NGAL concentrations in patients admitted to intensive care units (ICUs) and whether these determinations are directly comparable in this setting.
Methods
NGAL was measured in 40 paired samples of serum and EDTA plasma from 25 patients admitted to intensive care with a commercial particle‐enhanced turbidimetric immunoassay (The NGAL Test™, BioPorto Diagnostics A/S, Gentofte, Denmark) on a Roche Hitachi 917 (Roche‐Hitachi, Inc., Tokyo, Japan) analyzer.
Results
Serum NGAL concentrations ranged from 26.8 to 1,808 ng/ml (median 281 ng/ml, interquartile range (IQR) 453 ng/ml). EDTA plasma NGAL concentrations ranged from 25.7 to 1,752 ng/ml (median 225 ng/ml, IQR 352 ng/ml). The difference in NGAL concentrations in paired serum and EDTA plasma samples (serum– plasma) ranged from −13.8 to 321 ng/ml (median 79 ng/ml, IQR 116 ng/ml; difference from zero, P < 0.0001, Wilcoxon's signed rank test). Although serum and EDTA plasma values were correlated (Spearman's r = 0.95, P < 0.0001), Deming regression analysis showed a slope of 1.1 that was not significantly different from unity (95% confidence interval (CI) 1.0–1.1) and a highly significant intercept of 67.9 ng/ml with a wide confidence interval (95% CI 29.8–106).
Conclusion
NGAL concentration values measured in serum and EDTA plasma cannot be directly compared and should not be used as equivalents in studies of patients admitted to intensive care.
1 Department
of Medical Physiology, Panum Institute, University of Copenhagen,
DK-2200; and 2 Department of
Clinical Physiology, Herlev Hospital, University of
Copenhagen, DK-2730 Herlev, Denmark
...Effects of urodilatin (5, 10, 20, and 40 ng · kg 1 · min 1 )
infused over 2 h on separate study days were studied in eight normal subjects with use of a randomized, double-blind protocol. All doses
decreased renal plasma flow (hippurate clearance, 13-37%) and
increased fractional Li + clearance
(7-22%) and urinary Na +
excretion (by 30, 76, 136, and 99% at 5, 10, 20, and 40 ng · kg 1 · min 1 ,
respectively). Glomerular filtration rate did not increase
significantly with any dose. The two lowest doses decreased cardiac
output (7 and 16%) and stroke volume (10 and 20%) without changing
mean arterial blood pressure and heart rate. The two highest doses elicited larger decreases in stroke volume (17 and 21%) but also decreased blood pressure (6 and 14%) and increased heart rate (15 and
38%), such that cardiac output remained unchanged. Hematocrit and
plasma protein concentration increased with the three highest doses.
The renin-angiotensin-aldosterone system was inhibited by the three
lowest doses but activated by the hypotensive dose of 40 ng · kg 1 · min 1 .
Plasma vasopressin increased by factors of up to 5 during infusion of
the three highest doses. Atrial natriuretic peptide immunoreactivity (including urodilatin) and plasma cGMP increased dose dependently. The
urinary excretion rate of albumin was elevated up to 15-fold (37 ± 17 µg/min). Use of a newly developed assay revealed that baseline
urinary urodilatin excretion rate was low (<10 pg/min) and that
fractional excretion of urodilatin remained below 0.1%. The results
indicate that even moderately natriuretic doses of urodilatin exert
protracted effects on systemic hemodynamic, endocrine, and renal
functions, including decreases in cardiac output and renal blood flow,
without changes in arterial pressure or glomerular filtration rate, and
that filtered urodilatin is almost completely removed by the renal tubules.
atrial natriuretic factor; cardiac output; renal hemodynamics; sodium excretion; albuminuria
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).
Effects of urodilatin (5, 10, 20, and 40 ng-kg-1-min-1) infused over 2 h on separate study days were studied in eight normal subjects with use of a randomized, double-blind protocol.
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