The NANC system and airway vasculature

Widdicombe, J.G.

Archives Internationales de Pharmacodynamie et de Therapie 303: 83-99

1990


ISSN/ISBN: 0003-9780
PMID: 2196862
Document Number: 366073
The different structures of the nasal, tracheal and bronchial vascular beds are described. All the vasculatures are influenced by neuropeptides released from three types of nerve: (1) sympathetic nerves release both noradrenaline and neuropeptide Y (NPY), both of which cause vasoconstriction; (2) parasympathetic nerves release both acetylcholine and either vasoactive intestinal polypeptide (VIP), peptide histidine methionine (PHM) or peptide histidine isoleucine (PHI), all of which cause vasodilatation; and (3) sensory nerves release sensory neuropeptides such as substance P (SP), calcitonin gene-related peptide (CGRP) and neurokinins A and B (NKA, NKB). Direct application of the neuropeptides to various preparations of the vascular beds confirms their actions. Stimulation of nerves to the airways in vivo causes vascular changes in the presence of anti-acetylcholine, anti-noradrenaline and ganglionic-blocking drugs, suggesting that they are mediated by neuropeptides. Reflex activation of the parasympathetic and sympathetic nerves to the airway vasculature has been established, but the relative importance of classical neurotransmitters and of neuropeptides has not been analyzed. The neuropeptides in sensory nerves are released when the nerves are stimulated by capsaicin, various chemical irritants and inflammatory mediators such as histamine and bradykinin. The sensory neuropeptides cause not only vasodilatation but also, in some instances, extravasation of plasma protein and an increase in interstitial fluid volume. The interaction of the different neuropeptide systems, and their interplay with classical transmitters released from motor nerves, require further exploration.

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