Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P20366 (
substance P
)
21,176
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The bronchoconstriction caused by inhaled
neurokinin A
(
NKA
) in patients with asthma is indirect. The mediators involved in
NKA
-induced bronchoconstriction are unknown. Studies with various H1 receptor antagonists were negative, making an important contribution of histamine unlikely. To study the role of cysteinyl leukotrienes in
neurokinin A
-induced bronchoconstriction, we performed a randomised, double-blind, cross-over, placebo controlled trial in 12 patients with mild to moderate asthma.
Zafirlukast
and matching placebo were given orally, 40 mg the evening before and 40 mg the morning of assessment. In one period
NKA
was administered, in the other period leukotriene D4 (LTD4). Increasing concentrations of
NKA
and LTD4 were inhaled from a 30 L bag, after nebulization via a Mallinckrodt nebuliser. The difference between log10PC20LTD4 after treatment with placebo or zafirlukast was highly significant (p<0.0001). A trend was observed towards a difference between log10PC20
neurokinin A
after treatment with placebo or zafirlukast (p=0.0741). The dose ratio for the
neurokinin A
provocation was 4.4 and for the LTD4 provocation 67.7. In conclusion, zafirlukast had a large inhibitory effect on LTD4-induced bronchoconstriction, but offered only limited protective effect against
neurokinin A
-induced bronchoconstriction. We suggest that leukotrienes play a limited role in the bronchoconstrictor effect of
neurokinin A
in patients with asthma.
...
PMID:The effect of the leukotriene receptor antagonist zafirlukast on neurokinin A-induced bronchoconstriction in patients with asthma--A comparison with leukotriene D4 induced broncoconstriction. 1761 Nov 32