The role of sensory neuropeptides in the pathogenesis of bronchial asthma.

In recent years more than ten peptides have been demonstrated in mammalian lung. Some of them are present in the innervation of the mucosa, submucosa, smooth muscle and blood vessels and are called neuropeptides [1]. The neuropeptides vasoactive intestinal peptide (VIP) and substance P (SP) have been the best studied. They have been implicated as neurotransmitters of the non-adrenergic, non-cholinergic (NANC) airway innervation. A defect in this system could contribute to bronchial hyperresponsiveness, either by an increase in excitatory or by a decrease in inhibitory influences. The sensory neuropeptides substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide have been put forward as neurotransmitters of the local axon reflex. Experiments in rodents have indicated that the antidromic stimulation of axon collaterals of sensory nerve-endings can lead to bronchoconstriction and neurogenic airway inflammation by release of sensory neuropeptides in response to mechanical and chemical stimuli [2, 3]. The aim of the present study was to examine the bronchonconstrictor effect of these sensory neuropeptides in a rat model and to look for a possible role in human airways.