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Characterization of the neurogenic plasma extravasation in the airways.

Abstract
Release of neuropeptides from sensory nerves causes an increase in vascular permeability, plasma extravasation and edema. The sensory nerves in the airways can be activated by electrical stimulation of the vagus nerve or by application of chemical and mechanical irritants, such as capsaicin, hypertonic saline, isocapnic hyperpnea and cigarette smoke. In rodent airways, the neurogenic plasma extravasation is mediated by tachykinins released from the capsaicin-afferent nerve fibres, and involves activation of neurokinin-1 tachykinin receptors. In peripheral guinea-pig airways, neurokinin-2 tachykinin receptors have also been implicated in the neurogenic plasma exudation. The tachykinins can increase vascular permeability by both a direct effect on venular endothelium, and indirect mechanisms involving mast cell activation and serotonin release. Tachykinins and their receptors are present in the human airways. Release of tachykinins, following antigen challenge, has been demonstrated in the nose and lower airways. In humans, tachykinins have been shown to increase plasma exudation in the nasal mucosa, but whether neurogenic inflammation also occurs in the lower airways still remains to be proven.
AuthorsP R Germonpré, G F Joos, R A Pauwels
JournalArchives internationales de pharmacodynamie et de therapie (Arch Int Pharmacodyn Ther) 1995 Jan-Feb Vol. 329 Issue 1 Pg. 185-203 ISSN: 0003-9780 [Print] Belgium
PMID7543745 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Receptors, Tachykinin
  • Tachykinins
  • Substance P
  • Calcitonin Gene-Related Peptide
Topics
  • Animals
  • Calcitonin Gene-Related Peptide (pharmacology)
  • Capillary Permeability (drug effects)
  • Exudates and Transudates (physiology)
  • Humans
  • Neurons, Afferent (physiology)
  • Pulmonary Edema (physiopathology)
  • Receptors, Tachykinin (drug effects, physiology)
  • Respiratory System (drug effects, innervation)
  • Substance P (pharmacology)
  • Tachykinins (pharmacology)

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