Correction of hyperaldosteronism and of massive fluid retention of unknown cause by sympathomimetic agents

William B. Greenough, Edmund H. Sonnenblick, Vlodzimierz Januszewicz, John H. Laragh

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


A detailed study is reported of a thirty-nine year old woman with long-standing postural hypotension and recurrent episodes of massive anasarca. Later, periods of edema formation alternated with bouts of dehydration, azotemia and potassium depletion, and evidences of impaired renal function appeared. The episodes of sodium retention and edema formation were demonstrated to be associated with a marked increase in the adrenal secretory rate of aldosterone. The increased secretion of aldosterone was paradoxic because it occurred despite a relatively high sodium intake. Sustained diuresis was induced by a spirolactone dldosterone antagonist, providing evidence that aldosterone oversecretion was important in causation of the edematous state. Complete correction of the disorder during a prolonged period of observation was finally achieved by oral administration of sympathomimetic agents. Administration of these pressor agents produced a fall in the rate of secretion of aldosterone to normal values and a marked sodium diuresis. Potassium excretion did not increase. The nature of the disorder has not been elucidated. However, the patient was found to have hypervolemia and a markedly reduced glomerular filtration rate. It has been suggested that her arterial hypotension might be a result of venous pooling. The beneficial effects of the sympathomimetic drugs are viewed as a consequence of a direct or indirect action to improve the renal circulation, leading to suppression of the generation of an aldosterone stimulating factor (? angiotensin).

Original languageEnglish (US)
Pages (from-to)603-614
Number of pages12
JournalThe American journal of medicine
Issue number4
StatePublished - Oct 1962
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)


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