In 27 infants aged 20 to 65 days with clinically and roentgenologically proved hypertrophic pyloric stenosis gastric juice analyses were performed according to Lambling. Basic acid output and maximal acid output in these infants were significantly increased as compared to healthy infants of the same age group. The higher acid output in the hypertrophic pyloric stenosis group was due to higher volumes and a higher acidity of the gastric juices. Basic acid output and maximal acid output increased following pylorotomy. There is evidence, that hyperacidity in pylorus stenosis of infancy is primarily and not due to the pyloric constriction. There was a distinct correlation between the degree of metabolic alkalosis and diminished acid outputs. The findings support the thesis, that infantile hypertrophic stenosis is originated by an increased parietal cell mass. The increased acid secretion and the enhanced release of secretin and cholecystokinin are supposed to originate the hypertrophy of the pyloric muscle.