Zusammenfassung
In früheren eigenen Untersuchungen konnte erwiesen werden, daß eine wiederholte mäßige orale Flüssigkeitsbelastung an gesunden Versuchspersonen durch Hemmung der tubulären Reabsorption zu einer Steigerung der renalen Natriumausscheidung führt.
Zum Nachweis eines humoralen Faktors, der für diese Natriurese verantwortlich sein könnte, wurden durch Dialyse und Ultrafiltration gewonnene Fraktionen aus dem Urin derart vorbehandelter Versuchspersonen an natriumverarmten Ratten nach kombinierter oraler und intravenöser Belastung mit isotoner Kochsalzlösung auf ihre natriuretische Wirksamkeit untersucht. Der Urin wurde nach Einbringung der Tiere in Einzelstoffwechselkäfige 5 Std lang gesammelt, Urinvolumen, Natrium-, Chlorid- und Kaliumausscheidung wurden auf 100 g Körpergewicht/5 Std errechnet. Während die Kontrolltiere nahezu 50% des angebotenen Natrium retinieren (Na/K-Quotient 0,88), führt eine einzige i.v. Injektion von 25 µg MRL zum Anstieg der Natriumausscheidung. Die Kaliumausscheidung bleibt unverändert, der Na/K-Quotient erreicht einen Normwert von 2,0. Die negative freie Wasserclearance ist unter der Einwirkung von 25 µg des Urinextraktes signifikant reduziert. Daraus läßt sich auf eine Abnahme des anisosmotischen Natriumtransportes unter der Einwirkung des natriuretischen Prinzips schließen.
Die Ergebnisse weisen auf einen Rückgang der tubulären Natrium-Reabsorption hin und liefern den Beweis für die Existenz eines humoralen natriuretischen Faktors im Urin gesunder Versuchspersonen nach mäßiger oraler Flüssigkeitsbelastung.
Summary
Recently we demonstrated an increased renal sodium excretion without changes in tubular sodium load after moderate continuous oral hydration in normal man. To evaluate the possible existence of a humoral factor responsible for the natriuresis, urine preparations of hydrated normal persons were tested for natriuretic activity in a specially developed bioassay in rats. Urines were dialyzed and ultrafiltered. The lyophilized membrane residue was dissolved in isotonic saline. Sodium depleted rats received sodium in an amount of 750 µEq by gavage and 150 µEq intravenously. The animals were kept under standardized conditions in single metabolic cages. Urine was collected for five hours. Urine volume, osmolal clearance, sodium, chloride and potassium excretion were calculated for 100 g body weight/5 hours. Of the given sodium load, control animals retained almost 50% (mean: 222 of 470 µEq/100 g/5 hrs). Inspite of the sodium loading the urinary sodium: potassium ratio was reduced to 0.88. Intravenous injection of the urine preparations resulted in a dose-dependent decrease in the sodium retention with an increase in the sodium: potassium ratio to 2.0 at doses of 25 µg, potassium excretion being unaltered. The free water reabsorption was significantly reduced. The effect of this dose exceeded that of 50 µg of hydrochlorothiazide. The results point to a decrease of tubular sodium reabsorption and give evidence for the existence of a humoral natriuretic factor present in normal man after moderate oral hydration.
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Krück, F., Ressel, C. & Selb, D. Biologischer Nachweis eines humoralen natriuretischen Prinzips im Urin gesunder Menschen. Klin Wochenschr 45, 30–34 (1967). https://doi.org/10.1007/BF01745735
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DOI: https://doi.org/10.1007/BF01745735