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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
26
|
| pubmed:dateCreated |
1993-7-13
|
| pubmed:abstractText |
Salmeterol was developed to provide prolonged bronchodilatation to control nocturnal symptoms and improve maintenance therapy in asthmatic patients. Salmeterol is > 10,000 times more lipophilic than salbutamol and has greater affinity for the beta 2-adrenoceptor. Membrane binding is non-competitive and dissociation is slow so that its effects last for many hours. Despite this, salmeterol does not accumulate in tissues. Its mechanism of action can be explained by binding to a specific exo-site domain of the beta 2-receptor protein to produce continuous stimulation of the active site of the receptor, which gives salmeterol a profile of pharmacological activity unlike that of other beta 2-agonists. Due to its potent and prolonged activation of beta 2-adrenoceptors in airway smooth muscle cells, endothelial cells, mast cells and epithelial cells, salmeterol induces prolonged bronchodilatation, reduced vascular permeability, inhibition of inflammatory mediators, stimulation of ciliary function and modulation of ion and water transport across the bronchial mucosa.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:issn |
0024-3205
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
52
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
2131-43
|
| pubmed:dateRevised |
2005-11-16
|
| pubmed:meshHeading | |
| pubmed:year |
1993
|
| pubmed:articleTitle |
The pharmacology of salmeterol.
|
| pubmed:affiliation |
Department of Cardiovascular and Respiratory Pharmacology, Glaxo Group Research Ltd., Ware, Hertfordshire, England.
|
| pubmed:publicationType |
Journal Article,
Review
|