Abstract
Esophageal secretion of HCO −3 ions occurs in opossum and man and may contribute to mucosal defense. Using a perfusion technique, neuroregulatory influences on esophageal and salivary HCO −3 secretion were investigated in 24 healthy human subjects. The sight and smell of food increased median salivary HCO −3 output from 424 to 573 μmol/15 min (P=0.014), without significantly altering esophageal HCO −3 secretion (74–105 μmol/15 min,P=0.24). Atropine reduced both salivary (610 to 68, 17, 10, and 3 μmol/15 min in successive periods;P<0.028) and esophageal HCO −3 output (108 to 78, 35, 18, and 7 μmol/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 μmol/10 cm/15 min,P=0.036), implicating a noncholinergic mechanism. Cold-induced pain activated sympathetic reflexes and reduced esophageal HCO −3 output (91 to 64 μmol/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 HCO −3 secretion.
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Brown, C.M., Snowdon, C.F., Slee, B. et al. Neural influences on human esophageal and salivary alkali secretion. Digest Dis Sci 40, 1642–1650 (1995). https://doi.org/10.1007/BF02212684
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DOI: https://doi.org/10.1007/BF02212684