The nasal mucosa is the first internal surface to encounter aeroallergens, airborne pathogens, and airborne toxins. Analysis of nasal responses will likely provide insights into normal host defense mechanisms. Provocation of human and guinea pig nasal mucosa stimulates secretion, and analysis of the components of these secretions has revealed new insights into the source of these secretions as well as possible mechanisms for the pharmacologic control of secretion. Allergen challenge results in a direct vascular permeability due to mast cell derived mediators and reflex glandular secretions. An anti-inflammatory agent, nedocromil sodium, had no protective effect on responses caused by allergen. The three divisions of innervation in the nasal mucosa were found to have discrete associations with neuropeptides: the sensory nerves contain GRP (a glandular stimulant), CGRP, SP, and NKA (which act to regulate vasodilation and vascular permeability); the parasympathetic nerves contain VIP (a potent glandular stimulant); and sympathetic nerves contain NPY (a vasoconstrictor). Bradykinin, which may be generated during URls, was found to stimulate the vascular bed but not the glands directly; thus, bradykinin may participate in the vascular permeability seen in colds. Patients with recurrent sinusitis were found to have a singular defect in nasal secretory responses to cholinergic stimulation. Therefore, these patients may be predisposed to recurrent infections by the absence of specific and nonspecific host defense molecules. Uric acid was found to be the major, stable antioxidant in secretions. Uric acid secretion appeared to be glandular in origin.
