抄録
The respiratory tract is controlled by autonomic nerve systems. Besides cholinergic and adrenergic nerve systems, their is another efferent pathway, so-called non-adrenergic inhibitory nerve system (NAIS), in some species including human beings. Many kinds of neuropeptides, such as vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI), substance P (SP), neurokinin A (NKA) and clacitonin gene-related petide (CGRP), are now known to be present in the nerve systems of the respiratory tract. Among these peptides VIP and PHI are suggested to be the neurotransmitters of NAIS. Reversible bronchial obstruction and bronchial hyperreactivity are the outstanding clinical features of asthmatic patients. Neuropeptide may be involved in the process of the bronchial obstruction as follows. It has been reported that NKA may be the most important intrinsic bronchoconstrictor in the process because it effects as a more potent bronchoconstrictor on bronchial smooth muscle than SP in vitro. Axon-reflex might be present in the human respiratory tract as well as the skin and SP is suggested to be involved in this reflex. SP might be released with NKA and CGRP from primary afferent nerve endings and they could cause bronchoconstriction, mucus hypersecretion and inflammatory cells infiltration. On the contrary to the bronchoconstrictive action of these neuropeptides, VIP has been reported that it can dilate bronchial smooth muscle in asthmatics when given by intravenous infusion. Bronchial inflammation and the dysfunction of autonomic nerve systems in the bronchial smooth muscle are considered as the important factors of the pathogenesis of bronchial hyperreactivity. Dysfunction of NAIS caused by VIP and PHI degradation by proteases released from many inflammatory cells could be involved in the bronchial hyperreactivity.
