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Das Verhalten des Plasmaaldosterons und der Plasmareninaktivität bei primärer und renaler Hypertonie unter Stimulations- und Suppressionsbedingungen

Plasma aldosterone and plasma renin activity in patients with essential and renal hypertension under acute stimulation with saline depletion and acute suppression with saline infusion

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Summary

Plasma aldosterone, plasma renin activity, sodium and potassium in the plasma and the urine were determinated under acute stimulation with saline depletion (furosemide) and under acute suppression with saline infusion in 40 patients with primary hypertension stage I, 19 patients with primary hypertension stages II and III, and II patients with renal hypertension (chronic glomerulonephritis and chronic pyelonephritis). The majority of the patients with primary hypertension stage I showed a good stimulation of the plasma aldosterone and the plasma renin activity under acute salt depletion. Three out of the 40 patients with primary hypertension stage I, and 13 of the 19 patients with primary hypertension stages II and III did not show any stimulation of the renin secretion (“low renin hypertension”). In all these patients the plasma aldosterone stimulation remained intact. With infusion of saline all the groups showed suppression of the plasma aldosterone and the plasma renin activity. A good stimulation of the plasma aldosterone in spite of the lack of stimulation of the plasma renin activity, demonstrates that in our experiments the renin-angiotensin system cannot be responsible for the increase in aldosterone secretion under salt depletion. Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. In all patients with primary hypertension we did not find an inadequate reaction of the aldosterone secretion under saline infusion. The patients with renal hypertension showed a minimal stimulation and suppression of the plasma renin activity. The plasma aldosterone secretion increased only slightly under sodium depletion and the decrease under saline infusion was statistically not significant. Thus we conclude that these patients show an inadequate reaction of the plasma aldosterone and renin secretion under salt infusion and depletion.

Zusammenfassung

Bei 40 Patienten mit primärer Hypertonie Stadium I, 19 Patienten mit primärer Hypertonie Stadium II und III sowie bei 11 Patienten mit renaler Hypertonie (chronische Glomerulonephritis, chronische Pyelonephritis) wurde das Verhalten des Plasmaaldosterons, der Plasmareninaktivität sowie der Elektrolyte im Serum und Urin unter akuter Stimulation durch Salzentzug (Furosemid) und unter akuter Suppression durch Kochsalzinfusion geprüft. Die überwiegende Mehrzahl der Patienten mit primärer Hypertonie Stadium I zeigt eine gute Stimulierbarkeit des Plasmaaldosterons und der Plasmareninaktivität durch akuten Salzentzug. 3 von 40 Patienten mit primärer Hypertonie Stadium I und 13 von 19 Patienten mit primärer Hypertonie Stadium II und III hatten eine nicht stimulierbare Reninsekretion (“low renin hypertension”). Die Stimulierbarkeit des Plasmaaldosterons war jedoch bei allen diesen Patienten intakt. Unter Kochsalzbelastung fanden wir in allen Gruppen eine Supprimierbarkeit des Plasmaaldosterons und der Plasmareninaktivität. Die gute Stimulierbarkeit des Aldosterons bei Patienten mit fehlender Stimulierbarkeit der Plasmareninaktivität zeigt, daß unter unseren Versuchsbedingungen das Renin-Angiotensin-System bei Hochdruckkranken nicht für die gesteigerte Aldosteronsekretion bei Salzentzug verantwortlich sein kann. Wahrscheinlich erfolgt der Plasmaaldosteronanstieg bei Starre der Reninsekretion über den diuretikabedingten Natriumentzug. Ein inadäquates Verhalten der Aldosteronsekretion in Bezug auf akute Kochsalzbelastung besteht bei Patienten mit primärer Hypertonie nicht. Bei renoparenchymalem Hochdruck fand sich eine abgeschwächte Stimulierbarkeit und Supprimierbarkeit der Plasmareninaktivität. Das Plasmaaldosteron stieg auf Natriumentzug ebenfalls nur gering an und der Abfall nach Natriumchloridgabe war statistisch nicht signifikant. Beim renoparenchymalen Hochdruck liegt damit in Bezug auf Natriumchloridentzug und Natriumchloridzufuhr ein inadäquates Verhalten der Aldosteron- und Reninsekretion vor.

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  1. Medizinische Universitäts-Poliklinik Marburg, Germany

    F. Klumpp, D. Klaus, R. Lemke, J. Zehner & P. Zöfel

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  1. F. Klumpp
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Mit Unterstützung der Deutschen Forschungsgemeinschaft.

Zentrale Rechenanlage der Universität Marburg.

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Klumpp, F., Klaus, D., Lemke, R. et al. Das Verhalten des Plasmaaldosterons und der Plasmareninaktivität bei primärer und renaler Hypertonie unter Stimulations- und Suppressionsbedingungen. Klin Wochenschr 53, 221–229 (1975). https://doi.org/10.1007/BF01468811

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