The generation of experimental metabolic alkalosis by the kidney was found to require the presence of excess mineralocorticoid hormone and potassium deficiency. Once generated, metabolic alkalosis could be maintained in the absence of excess mineralocorticoid, provided a strong stimulus (extracellular volume contraction or potassium deficiency or both) to proximal reabsorption was present. When proximal reabsorption was not markedly stimulated, metabolic alkalosis was corrected on reduction or discontinuance of mineralocorticoid; under these circumstances correction of potassium deficiency also corrected metabolic alkalosis. The development of metabolic alkalosis by the kidney requires accelerated distal tubular Na for H exchange. This mechanism may also maintain metabolic alkalosis as may increase proximal H+ secretion.
Neil A. Kurtzman, Martin G. White, Philip W. Rogers. Pathophysiology of Metabolic Alkalosis. Arch Intern Med. 1973;131(5):702–708. doi:10.1001/archinte.1973.00320110086013