Clinical study
The response of normal man to selective depletion of hydrochloric acid: Factors in the genesis of persistent gastric alkalosis

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Abstract

Factors responsible for the development of gastric alkalosis in man have been examined by means of selective depletion of hydrochloric acid without concomitant extrarenal depletion of sodium, potassium or water. Throughout the study the subjects ingested a diet of normal composition except for its low sodium and chloride content. In each instance the removal of hydrochloric acid led to the development of persistent metabolic alkalosis (plasma bicarbonate concentration 34 to 39, mEq. per L.), and augmented renal potassium excretion. There was little or no change in sodium balance. The constancy of the glomerular filtration rate and of serum sodium concentration indicate not only that the renal threshold for bicarbonate was elevated but also that the rate of sodium-hydrogen exchange was accelerated.

The data demonstrate that an extrarenal loss of sodium, potassium and water during vomiting or gastric drainage in man is not a prerequisite to the development of sustained metabolic alkalosis or potassium deficiency. It is evident that the observed cation and water deficits develop as the result of secondary renal adjustments to hypochloremia. The characteristics of a mechanism which appears to account for these renal adjustments have been considered.

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This study was supported in part by Grants H-759 and HTS-5309 from the National Heart Institute, National Institutes of Health, Public Health Service, Public Health Service Grant FR 54, General Clinical Research Centers Branch, National Institutes of Health, and the Samuel Bass Fund for Kidney Research.

1

From the Department of Medicine, Tufts University School of Medicine, and the Renal Service, Pratt Clinic-New England Medical Center Hospitals, Boston, Massachusetts.

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