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Abstract
Epidermal growth factor (EGF) has recently been localized in salivary, pancreatic, and Brunner's glands in humans, but little is known about its release and its action on gastric secretion. This study, performed on healthy subjects, was designed to determine the release of immunoreactive EGF in plasma and in salivary and gastric secretions under basal conditions and after modified sham feeding (MSF), ordinary feeding, and infusion of pentagastrin without and with addition of exogenous recombinant human EGF (hEGF). Under basal conditions the EGF concentrations in plasma and salivary and gastric secretions were 52 ± 8 pg/ml, 2.5 ± 0.3 ng/ml, and 0.12 ± 0.03 ng/ml, respectively. MSF and ordinary feeding increased significantly EGF plasma level and salivary output but not gastric EGF output, and atropinization failed to affect these plasma and salivary EGF responses to MSF. Intravenous infusion of pentagastrin increased both plasma and salivary but not gastric EGF, and addition of exogenous hEGF in graded doses (0.25–1.0 μg/kg) resulted in a dose-dependent increase in the plasma level of EGF and in significant inhibition of gastric acid and pepsin outputs. The increment in plasma EGF, which resulted in significant inhibition of gastric secretion, was several times greater than that observed after MSF or feeding. EGF infused in a constant dose (0.12 or 1.0μg/kg-h) caused significant inhibition of the gastric acid response to MSF only in the higher dose and not in the lower dose, although the latter (0.12μg/kg-h) resulted in an increment in plasma EGF similar to that observed after MSF alone. Mean disappearance half-life of plasma EGF on stopping the EGF infusion was 8.7 ±2.1 min. We conclude that in humans 1) the release of EGF into the circulation and saliva remains under neurohormonal control; 2) exogenous EGF causes a potent and dose-related inhibition of gastric secretion which is closely related to the increment in plasma EGF levels; and 3) endogenous EGF released postprandially seems unlikely to contribute to the control of gastric acid secretion.