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Regulation der Plasmaaldosteronkonzentration bei nierenlosen Patienten

Regulation of aldosterone secretion in anephric patients

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Summary

The influence of ACTH, angiotensin II, orthostasis and hemodialysis on plasma aldosterone concentration was investigated in 14 anephric patients. Furthermore, plasma renin activity (PRA), plasma cortisol, plasma sodium concentration and plasma potassium concentration were measured.

After infusion of synthetic ACTH (2.5 εg/min Synacthen) for 4 h a significant rise of plasma aldosterone concentration and plasma cortisol concentration was observed (p<0.025,p<0.005, respectively), whereas serum sodium and serum potassium concentrations remained unchanged.

A slight though not statistically significant rise of plasma aldosterone concentrations was observed after 1 h-infusion of synthetic angiotensin II (1.0 ng/kg/min Hypertensin) while plasma cortisol concentration and serum electrolytes showed only minor changes. Sixty min after starting the infusion with angiotensin II ACTH (2.5 µg/min Synacthen) was infused additionally over a period of 4 h. Under the latter conditions as with ACTH alone an increase of plasma aldosterone concentration was observed.

Orthostasis caused a significant rise in plasma aldosterone (p<0.05), whereas plasma cortisol and the serum electrolytes remained unchanged.

Conventional as well as isonatriaemic and isokaliaemic hemodialysis let to a comparable increase of plasma aldosterone. Plasma cortisol was unchanged during conventional hemodialysis, and showed a decrease after isonatriaemic and isokaliaemic hemodialysis.

With a few exceptions plasma renin activity (PRA) was undetectable low (<0.2 ng/ml·3 h). In those instances where low normal PRA values were found, these values were not influenced by hemodialysis or orthostasis.

Our results show that in anephric patients plasma aldosterone increased in response to synthetic ACTH, orthostasis and hemodialysis. After the infusion of angiotensin II only a slight, statistically not significant increase in plasma aldosterone concentration was observed. The simultaneous infusion of ACTH and angiotensin II let to a comparable increase in plasma aldosterone as ACTH alone.

Furthermore, hemodialysis let to an increase of plasma aldosterone under conventional as well as under isokaliaemic and isonatriaemic conditions. These changes in hormone concentration as well as those induced by orthostasis could not be explained by one of the known aldosterone stimulating factors. Thus, our findings suggest that other factors may be involved in the regulation of plasma aldosterone in anephric man.

Zusammenfassung

Bei 14 anephrischen Patienten wurde der Einfluß von ACTH, Angiotensin II, Orthostase und Hämodialyse auf die Plasmaaldosteronkonzentration untersucht. Gleichzeitg wurden Plasmareninaktivität (PRA), Plasmacortisol, Serumnatrium und Serumkalium bestimmt.

Unter 4stündiger Infusion von synthetischem ACTH (2,5 µg/min Synachten) kam es zu einem signifikanten Anstieg des Plasmaaldosterons und des Plasmacortisols (p<0,025 bzw. <0,005), während Serumnatrium und Serumkalium unverändert blieben.

Eine einstündige Infusion einer suppressorischen Dosis von synthetischem Angiotensin II (1,0 ng/kg Körpergewicht/min Hypertensin) führte zu einem geringgradigen, jedoch nicht signifikanten Anstieg des Plasmaaldosterons und hatte keinen Einfluß auf Plasmacortisol und Serumelektrolyte. Eine nach 60 min zusätzlich durchgeführte ACTH-Infusion (2,5 µg/min Synacthen) bewirkte über einen Zeitraum von 4 h einen ähnlichen Plasmaaldosteronansteig wie die alleinige ACTH-Infusion.

Durch Orthostase ließ sich ein signifikanter Anstieg des Plasmaaldosterons (p<0,05) erzielen, während Plasmacortisol und Serumelektrolyte keine signifikanten Veränderungen zeigten.

Sowohl normale als auch isonatriämische und isokaliämische Hämodialyse führten zu einem vergleichbaren Anstieg des Plasmaaldosterons. Das Plasmacortisol blieb bei der normalen Hämodialyse unverändert und fiel bei der isonatriämischen und isokaliämischen Hämodialyse ab.

Die Plasmareninaktivität war unter den beschriebenen Versuchsbedingungen mit ganz wenigen Ausnahmen nicht meßbar (<0,2 mg/ml·3 h). Vereinzelt tiefnormale PRA-Werte wurden weder durch Hämodialyse noch Orthostase beeinflußt.

Unsere Ergebnisse zeigen bei nierenlosen Patienten eine Stimulation des Plasmaaldosterons durch synthetisches ACTH, ein geringgradiges Ansprechen auf suppressorisches Angiotensin II, eine fehlende Potenzierung der ACTH-Wirkung durch suppressorische Dosen von Angiotensin II und einen Aldosteronanstieg unter Orthostase. Ferner ließ sich unter Hämodialyse ein Anstieg des Plasmaaldosterons beobachten. Dieser Anstieg trat sowohl unter normaler als auch unter isokaliämischer und isonatriämischer Hämodialyse auf und konnte deshalb ebenso wie die durch Orthostase induzierte Veränderung der Hormonkonzentration keinem der bekannten aldosteronstimulierenden Faktoren zugeordnet werden. Eine mögliche Beteiligung anderer Faktoren an der Aldosteronregulation ist deshalb anzunehmen.

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Authors and Affiliations

  1. Hämodialysestation Stadtspital Waid Zürich, Switzerland

    J. Tuma, K. Záruba, A. Studer, T. Lüscher, W. Siegenthaler, H. Vetter &  W. Vetter

  2. Medizinische Universitätspoliklinik Münster, Germany

    J. Tuma, K. Záruba, A. Studer, T. Lüscher, W. Siegenthaler, H. Vetter &  W. Vetter

  3. Dept. f. Innere Medizin, Universitätsspital, CH-8091, Zürich, Schweiz

    J. Tuma, K. Záruba, A. Studer, T. Lüscher, W. Siegenthaler, H. Vetter &  W. Vetter

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Tuma, J., Záruba, K., Studer, A. et al. Regulation der Plasmaaldosteronkonzentration bei nierenlosen Patienten. Klin Wochenschr 59, 27–34 (1981). https://doi.org/10.1007/BF01477327

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