The Role of Chloride in Hypokalemic Alkalosis in the Rat*

Abstract

Rats were made potassium deficient and alkalotic by dietary restriction of K and, in part of the experiments, by the intraperitoneal administration of desoxycorticosterone gluconate. The changes in whole body inulin space and in electrolytes of plasma, whole body, muscle, and skin were studied during chronic or during acute administration of KC1 or KNO3 K-deficient animals exhibited a K deficit of approximately 20% or normal carcass content. Changes in K and Na as a result of K deficiency were nearly wholly confined to muscle. Changes in skin were of minor importance. In the K-deficient animals a Cl deficit of approximately 2.8 mEq per 100 g fat-free dry solids was found, corresponding to 7.6 mEq per kg fat-free wet weight. There was no significant difference either in inulin spaces or in Cl spaces between K-deficient and completely repleted animals. It was not possible to fully correct either hypocloremic alkalosis or K deficiency without the administration of Cl. Administration of K as Cl or as HCO3 increased renal chloride reabsorption. On acute administration of K salt to functionally nephrectomized rats the penetration of K into muscle cells was not influenced by the plasma Cl concentration. The results demonstrate the critical role of chloride in the recovery and probably in the pathogensis of extracellular alkalosis in the K-deficient rat.