Advertisement
Free access | 10.1172/JCI107001
Endocrine-Metabolic Unit, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Dluhy, R. in: JCI | PubMed | Google Scholar
Endocrine-Metabolic Unit, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Axelrod, L. in: JCI | PubMed | Google Scholar
Endocrine-Metabolic Unit, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Underwood, R. in: JCI | PubMed | Google Scholar
Endocrine-Metabolic Unit, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Williams, G. in: JCI | PubMed | Google Scholar
Published August 1, 1972 - More info
The responses of plasma aldosterone, cortisol, and corticosterone to an infusion of 75 mEq of potassium chloride over 120 min were studied in 10 normal subjects. Five subjects were fed a 10 mEq and five a 200 mEq sodium diet, while all subjects ingested 40 mEq and 200 mEq potassium sequentially. Two potassium infusions were performed in each subject when in balance on a fixed sodium intake and low and then high potassium diets.
Regardless of dietary intake, increases of serum potassium of 0.5-1.5 mEq/liter above preinfusion levels were usually associated with significant increments in plasma aldosterone concentration. Our data agree with previous evidence that the potassium ion stimulates the adrenal cortex directly to secrete aldosterone. Peripheral renin activity did not increase after the potassium infusion. Plasma cortisol and corticosterone levels generally followed the expected diurnal decline during the infusion, implying that ACTH secretion did not increase.
The plasma aldosterone response to incremental changes in serum potassium was linear on each of the four diets. The slopes of these linear relationships increased significantly when the potassium intake was increased from 40 to 200 mEq. No increase in slope occurred on either potassium intake when dietary sodium was restricted from 200 to 10 mEq. Thus, identical increases in serum potassium were associated with greater increments in plasma aldosterone above preinfusion levels on either sodium intake when the 200 mEq potassium diet was compared with the 40 mEq potassium intake.