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A B S T R A C T Bolus injections of gastrin or pentagastrin (PG) cause a marked elevation in lower esophageal sphincter pressure (LESP), and it has been suggested that serum gastrin concentration is the main physiological and pathophysiological regulator of LESP. We evaluated this hypothesis by measuring LESP and gastric acid secretion simultaneously in normal subjects during continuous infusion of PG (0.004-12 /Lg/ kg per h), since continuous infusion of a hormone probably simulates physiological hormone release better than bolus injection. In groups of 8-13 subjects there was no statistically significant increase in average LESP with any of seven PG infusion rates. However, a bolus of PG superimposed on the continuous infusion of PG resulted in a 20-mm Hg increase in LESP. Examination of results in individual subjects suggested that PG by infusion might be stimulating LESP in some subjects and inhibiting it in others. Therefore, individual dose-response studies were performed in two normal subjects. These revealed that 0.9 /Ag/kg per h PG by infusion elevated LESP by 10-12 mm Hg. This dose of PG also elicited maximal rates of gastric acid secretion. In one of the subjects an infusion of PG calculated to give one-half maximal acid secretion (Dw) elevated LESP by 8 mm Hg; in the other the PG-D6o for acid secretion had no effect on sphincter pressure. Infusion of smaller amounts of PG had no effect on LESP, even though gastric acid secretion was stimulated submaximally.Preliminary results of this study were reported in abstract form in Gastroenterology. 1973. 64

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