NEURAL INFLUENCES ON HUMAN ESOPHAGEAL AND SALIVARY ALKALI SECRETION

Esophageal secretion of HCO3- ions occurs in opossum and man and may contribute to mucosal defense. Using a perfusion technique, neuroregulatory influences on esophageal and salivary HCO3- secretion were investigated in 24 healthy human subjects. The sight and smell of food increased median salivary HCO3- output from 424 to 573 mu mol/15 min (P = 0.014), without significantly altering esophageal HCO3- secretion (74-105 mu mol/15 min, P = 0.24). Atropine reduced both salivary (610 to 68, 17, 10, and 3 mu mol/15 min in successive periods; P < 0.028) and esophageal HCO3- output (108 to 78, 35, 18, and 7 mu mol/10 cm/15 min; P < 0.028), respectively. Following atropinization, cholinergic stimulation failed to increase salivary secretion but did ''unmask'' a small rise in esophageal alkali output (7 to 27 mu mol/10 cm/15 min, P = 0.036), implicating a noncholinergic mechanism. Cold-induced pain activated sympathetic reflexes and reduced esophageal HCO3- output (91 to 64 mu mol/10 cm/15 min, P = 0.041) without influencing salivary secretion. These observations support a role for the autonomic nervous system in modulating human esophageal and salivary HCO3- secretion.