Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the effects of parainfluenza virus type 3 (PI-3) on sensory neuropeptide levels, tachykinin receptors and their functions in guinea pig airways during the course of respiratory viral infection. PI-3 infected guinea pigs were hyperresponsive to methacholine and substance P aerosols as determined by earlier onset of dyspnea in these animals as compared with control on post-inoculation day (PID) 7 but not 19. In addition, plasma protein extravasation produced in response to the tachykinin was increased in infected airways during the first week post inoculation. Infected guinea pig trachea did not respond any differently to methacholine when smooth muscle contraction and [3H]inositol phosphate accumulation were measured although the magnitude of substance P effects using in vitro tests was significantly greater than control on post-inoculation day 7 but not 19. Trachea from PI-3 infected animals were characterized by reductions in substance P-like immunoreactivity, tachykinin NK1 receptor number and agonist affinity during the first post-inoculation week. Substance P levels or tachykinin NK1 receptor numbers or affinity were not altered in trachea of guinea pigs 4 days after treatment with lipopolysaccharide. These data suggest substance P release occurs during critical periods of respiratory viral infection which are temporally correlated with airway hyperresponsiveness. Despite apparent down-regulation of tachykinin NK1 receptors, substance P-mediated functions remained enhanced suggesting some alterations in post-receptor mechanisms.
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PMID:Parainfluenza virus type 3 induced alterations in tachykinin NK1 receptors, substance P levels and respiratory functions in guinea pig airways. 752 81

Rats are increasingly used to study airway inflammation and bronchial responsiveness. Relative little is known on the contribution of small airways in this animal model. We therefore compared the responsiveness to various inflammatory agents of isolated trachea, main bronchi (using classic organ bath) and isolated bronchioles (using small myograph) from Wistar and Fisher 344 rats. The largest contraction was elicited on all preparations by carbachol. Histamine elicited a (small) contraction only on bronchioles. The contractions elicited by serotonin, bradykinin, and the thromboxane A2-mimetic U-46619 were always relatively larger in bronchioles than in trachea and main bronchi. The sensitivities to carbachol and serotonin were smaller in bronchioles. The tachykinins substance P and neurokinin A elicited no substantial contraction on bronchioles or main bronchi. Trachea of Fisher 344 but not of Wistar rats showed a small contraction. No other differences were found between preparations from Wistar and Fisher 344 rats. It is concluded that rat trachea, main bronchi and small bronchioles show regional and strain-dependent variations in their responsiveness to contractile agents.
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PMID:Regionally different influence of contractile agonists on isolated rat airway segments. 971 2