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Research Article Free access | 10.1172/JCI105769
15th and 6th (Boston University) Medical Services, Boston City Hospital, and the Department of Medicine, Boston University School of Medicine, Boston University Medical Center, Boston, Massachusetts 02118
Find articles by Alexander, E. in: JCI | PubMed | Google Scholar
15th and 6th (Boston University) Medical Services, Boston City Hospital, and the Department of Medicine, Boston University School of Medicine, Boston University Medical Center, Boston, Massachusetts 02118
Find articles by Levinsky, N. in: JCI | PubMed | Google Scholar
Published April 1, 1968 - More info
Rats fed a diet high in potassium for several days survive an acute load of potassium that is lethal to animals on a regular diet. Previous data suggested that this survival occurred because of enhanced kaluresis.
Although increased urinary excretion may occur, the major mechanism of this potassium adaptation phenomenon has been found to be extrarenal. Despite nephrectomy just before study, rats previously fed a high potassium diet maintained lower plasma potassium concentrations for at least 2 hr after an acute potassium load than did rats fed a regular diet.
Prior adrenalectomy abolished adaptation. Furthermore, rats fed a low sodium diet as an alternative stimulus to aldosterone secretion demonstrated adaptation to potassium loading, as did adrenalecomized rats given large doses of deoxycorticosterone for several days. Adrenalectomy just before the test load of potassium did not abolish adaptation nor did a large dose of aldosterone at that time reproduce it. These data indicate that adaptation is dependent on a chronic increase in aldosterone secretion.
The extra potassium removed from the extracellular fluid by adapted rats was not lost into the gastrointestinal tract. It is concluded that more rapid lowering of plasma potassium after acute potassium loads by adapted rats is due to enhanced uptake of potassium by one or more tissues stimulated by chronic aldosteronism.