Linked Life Data

1693365

Source:http://linkedlifedata.com/resource/pubmed/id/1693365

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1990-7-11
pubmed:abstractText
In the guinea pig isolated perfused lung, we have examined the relationship between the effects of capsaicin and neuropeptide release and the possible existence of an axon reflex arrangement. Bolus injections into the pulmonary artery of capsaicin (1-100 pmol), substance P (10-1,000 pmol), and neurokinin (NK) A (10-100 pmol) produced a concentration-dependent bronchoconstriction, whereas calcitonin gene-related peptide (CGRP, 20-40 nmol) was without effect. Repeated administration of capsaicin at 40- to 60-min intervals was not associated with tachyphylaxis. These data support the presence of a NK2- (or NKA) type of tachykinin receptor in the guinea pig airways. Tetrodotoxin (0.3-3 microM) inhibited the effect of capsaicin, indicating that an axon reflex was operant. Capsaicin increased overflow of CGRP-like immunoreactivity (-LI) and NKA-LI, the latter only during concurrent infusion of the enkephalinase inhibitor phosphoramidon (3 microM). Phosphoramidon also increased overflow of CGRP-LI, suggesting that both NKA and CGRP were catabolized by a similar enzyme. The purine nucleoside adenosine did not cause any detectable overflow of CGRP-LI, indicating that neuropeptides may not be involved in adenosine-evoked bronchoconstriction and that bronchoconstriction per se does not induce neuropeptide overflow. Capsaicin and NKA had only minor effects on buffer flow, whereas substance P produced pulmonary vasoconstriction. These data clearly demonstrate that capsaicin acts via an axon reflex in the guinea pig airways. Supramaximal concentrations of capsaicin are needed to detect neuropeptide overflow, but the possibility exists that released neuropeptides mediate its effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1679-87
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1693365-Acetylcholine, pubmed-meshheading:1693365-Adenosine, pubmed-meshheading:1693365-Airway Resistance, pubmed-meshheading:1693365-Animals, pubmed-meshheading:1693365-Bronchi, pubmed-meshheading:1693365-Calcitonin Gene-Related Peptide, pubmed-meshheading:1693365-Capsaicin, pubmed-meshheading:1693365-Constriction, Pathologic, pubmed-meshheading:1693365-Dose-Response Relationship, Drug, pubmed-meshheading:1693365-Drug Interactions, pubmed-meshheading:1693365-Glycopeptides, pubmed-meshheading:1693365-Guinea Pigs, pubmed-meshheading:1693365-Hydrogen-Ion Concentration, pubmed-meshheading:1693365-Lung, pubmed-meshheading:1693365-Lung Compliance, pubmed-meshheading:1693365-Male, pubmed-meshheading:1693365-Neurokinin A, pubmed-meshheading:1693365-Neuropeptides, pubmed-meshheading:1693365-Substance P, pubmed-meshheading:1693365-Tetrodotoxin
pubmed:year
1990
pubmed:articleTitle
Capsaicin-induced bronchoconstriction and neuropeptide release in guinea pig perfused lungs.
pubmed:affiliation
Department of Clinical Pharmacology, University Hospital of Lund, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't