The human airway is richly innervated by peptidergic nerves, which help to regulate several aspects of airway function, including bronchomotor tone (1-5), glandular secretion (6, 7), vascular permeability and tone (8, 9), and neurogenic inflammation (10, 11). Histologic observations confirm that mast cells are often in close proximity to nerves (12-16). As a result of this close anatomic association, neural discharge may cause mast cell degranulation (17, 18). The stimulated release of mast cell mediators, particularly their secretory peptidases, may in turn modulate neuropeptide effects. Evidence of a role for mast cell peptidases in regulating neuropeptide effects was provided recently by in vivo studies of interactions between substance P (SP) and calcitonin generelated peptide (CGRP) in human and rat skin (19, 20). Other evidence of such a role derives from in vitro studies that demonstrate that the dog mast cell proteases tryptase and chymase rapidly hydrolyze vasoactive intestinal peptide