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Angiotensin stimulated AVP-release in humans

Angiotensin-stimulierte ADH-Freisetzung beim Menschen

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Summary

Release of arginine vasopressin (AVP) from rat neurohypophysis in in vitro studies is significantly augmented by the addition of angiotensin (AII), and in in vivo studies in dogs renin and AII were found to stimulate secretion of AVP. Both these results suggest the existence of a direct relationship between the salt regulating renin-angiotensin-aldosterone system and the water controlling AVP system.

To evaluate whether such observations apply also in man a sensitive double antibody radioimmunoassay for AVP was developed [17, 18].

Basal plasma levels of AVP in recumbent humans without salt and fluid restriction at room temperature were 3.4±2.2 pg/ml, and 30 min after the onset of an AII infusion at a concentration of 3–30ng/min·kg, a significant increase of AVP was found. Maximum measurements were 2–5 times basal levels which returned to normal within 90 min. During the AII infusion one also noted a 20 mm Hg rise in blood pressure, accompanied by a significant decrease in plasma renin activity. During the same period serum osmolality and serum sodium concentration did not change. Elevation of blood pressure by norepinephrine was not followed by any detectable change of plasma AVP levels, thus excluding a nonspecific blood pressure effect.

Zusammenfassung

In vitro wird die Freisetzung von ADH aus der Neurohypophyse der Ratte durch Zugabe von Angiotensin (AII) signifikant gesteigert; entsprechend ist am Hund in vivo eine Stimulation der ADH-Abgabe nach AII nachweisbar. Beides läßt auf eine enge Beziehung des Renin-Angiotensin-Aldosteron-Systems mit ADH schließen.

Um auch beim Menschen nähere Aussagen hierüber zu gewinnen, wurde ein sensitiver Radioimmunoassay für ADH entwickelt [17, 18].

Die gemessenen basalen ADH-Werte entsprechen den in der Literatur mitgeteilten Daten und betragen 3,4±2,2 pg/ml. Nach AII-Infusion (3–30 ng/min·kg) kommt es zu einem signifikanten Anstieg auf das 2–5fache des Ausgangswertes. Innerhalb von 90 min kehren die Werte wieder auf den Ausgangsbetrag zurück. Zur Kontrolle eines wirksamen AII-Spiegels diente die Erhöhung des Blutdruckes um ca. 20 mm Hg. Der Plasmareninwert nahm innerhalb dieser Zeit ab, Osmolalität und Elektrolytkonzentration des Plasmas änderten sich nicht. Eine Freisetzung von ADH durch die Erhöhung des Blutdruckes per se scheint äußerst unwahrscheinlich zu sein, da bei der zu gleichem Druckanstieg führenden Gabe von Noradrenalin keine Erhöhung des ADH-Spiegels im Plasma gefunden wurde.

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Authors and Affiliations

  1. II. Medizinische Universitätsklinik München, Germany

    E. Uhlich, P. Weber, J. Eigler & U. Gröschel-Stewart

  2. Universitäts-Frauenklinik Würzburg, Germany

    E. Uhlich, P. Weber, J. Eigler & U. Gröschel-Stewart

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  1. E. Uhlich
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  2. P. Weber
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  3. J. Eigler
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  4. U. Gröschel-Stewart
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Uhlich, E., Weber, P., Eigler, J. et al. Angiotensin stimulated AVP-release in humans. Klin Wochenschr 53, 177–180 (1975). https://doi.org/10.1007/BF01466762

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