EXPERIMENTAL POTASSIUM DEPLETION IN NORMAL HUMAN SUBJECTS. II. RENAL AND HORMONAL FACTORS IN THE DEVELOPMENT OF EXTRACELLULAR ALKALOSIS DURING DEPLETION*
Open Access
- 1 July 1959
- journal article
- research article
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 38 (7) , 1149-1165
- https://doi.org/10.1172/jci103891
Abstract
Three normal male human subjects were depleted of K in 4 balance studies using a treated milk diet containing less than 1 meq of K and up to 350 meq Na/day (with a chloride-bicarbonate ratio of 3:1). A 20 mg dose of desoxycorticosterone (DCA)/ day was given to each subject on the last 5 or 6 days of each study. Potassium deficits ranged from 288 to 618 meq/subject (221 to 502 when corrected for N balance), the rate of K loss in stool and urine being increased by DCA. Urinary pH showed only small changes but the excretion of NH4+ increased; the renal excretion of total acid was diminished relative to the excretion calculated as necessary to maintain external acid balance prior to DCA and was relatively increased during DCA administration. Hypokalemia developed in all 4 subjects, a slight tendency to extracellular metabolic alkalosis appeared in 2 subjects, and a substantial alkalosis occurred in a 3d. Derived data showed about a 2:3 ratio for the exchange of extracellular Na for intracellular K (relative to chloride space) in all subjects and roughly a 1:1 ratio for replacement by H of the cellular deficit of K over N in 3 of the subjects; in the 4th, intracellular retention of H was greatly in excess of this portion. It is concluded that K depletion due to dietary deprivation of normal human subjects results in: (1) partial replacement by Na of the cellular K deficit in the approximate ratio of 2:3; (2) a more widely variable shift of H from the extracellular phase with resultant extracellular deficit of H or excess of HCO3- and buffer anions; (3) a tendency for the changes in renal acid excretion to affect more the acid content of the intracellular rather than of the extracellular phase; and (4) development of extracellular metabolic alkalosis in terms of a rise in concentration of HCO3- and total buffer anion depending upon the associated change in extracellular volume and the net effect of the above internal ionic shifts.Keywords
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