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Article: Calcium channel blockers and asthma

TitleCalcium channel blockers and asthma
Authors
Issue Date1986
PublisherSpringer New York LLC. The Journal's web site is located at http://link.springer.de/link/service/journals/00408/
Citation
Lung, 1986, v. 164 n. 1, p. 1-16 How to Cite?
AbstractAn increase in cytoplasmic Ca ++ concentration can activate not only respiratory smooth muscles, but also mast cells, bronchial mucus glands, and the vagi. Altered control of cytoplasmic Ca ++ may also be related to the development of bronchial hyperreactivity. Drugs that block Ca ++ influx through specific Ca ++ channels in plasma membranes are therefore expected to be effective in the treatment of asthma. Reports so far indicate that such drugs may enhance the action of bronchodilators and may offer partial protection against histamine- or methacholine-induced bronchoconstriction; but they neither modify the basal bronchomotor tone of asthmatics nor reverse established bronchoconstriction. Calcium-channel blockers are also weak inhibitors of mediator release from mast cells except at high concentrations, which partially explains their inconsistent blocking activity in allergen-induced asthma. However, they are usually effective in preventing exercise-induced bronchoconstriction. They offer alternative treatment for patients with chronic airflow obstruction who need β-adrenergic blockade for coexisting cardiovascular problems. Limited data suggest that long-term use of calcium-channel blockers may benefit patients with chronic asthma. The therapeutic role of currently available Ca ++-channel blockers is limited in asthma in view of their low potency; more specific airway Ca ++ antagonists need to be developed.
Persistent Identifierhttp://hdl.handle.net/10722/161707
ISSN
2015 Impact Factor: 2.0
2015 SCImago Journal Rankings: 0.785
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSo, SYen_US
dc.contributor.authorIp, Men_US
dc.contributor.authorLam, WKen_US
dc.date.accessioned2012-09-05T05:14:13Z-
dc.date.available2012-09-05T05:14:13Z-
dc.date.issued1986en_US
dc.identifier.citationLung, 1986, v. 164 n. 1, p. 1-16en_US
dc.identifier.issn0341-2040en_US
dc.identifier.urihttp://hdl.handle.net/10722/161707-
dc.description.abstractAn increase in cytoplasmic Ca ++ concentration can activate not only respiratory smooth muscles, but also mast cells, bronchial mucus glands, and the vagi. Altered control of cytoplasmic Ca ++ may also be related to the development of bronchial hyperreactivity. Drugs that block Ca ++ influx through specific Ca ++ channels in plasma membranes are therefore expected to be effective in the treatment of asthma. Reports so far indicate that such drugs may enhance the action of bronchodilators and may offer partial protection against histamine- or methacholine-induced bronchoconstriction; but they neither modify the basal bronchomotor tone of asthmatics nor reverse established bronchoconstriction. Calcium-channel blockers are also weak inhibitors of mediator release from mast cells except at high concentrations, which partially explains their inconsistent blocking activity in allergen-induced asthma. However, they are usually effective in preventing exercise-induced bronchoconstriction. They offer alternative treatment for patients with chronic airflow obstruction who need β-adrenergic blockade for coexisting cardiovascular problems. Limited data suggest that long-term use of calcium-channel blockers may benefit patients with chronic asthma. The therapeutic role of currently available Ca ++-channel blockers is limited in asthma in view of their low potency; more specific airway Ca ++ antagonists need to be developed.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://link.springer.de/link/service/journals/00408/en_US
dc.relation.ispartofLungen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAsthma - Drug Therapy - Physiopathologyen_US
dc.subject.meshBronchi - Drug Effects - Physiopathologyen_US
dc.subject.meshBronchodilator Agentsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channel Blockers - Pharmacology - Therapeutic Useen_US
dc.subject.meshCell Adhesionen_US
dc.subject.meshCinnarizine - Therapeutic Useen_US
dc.subject.meshDogsen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHistamine Releaseen_US
dc.subject.meshHumansen_US
dc.subject.meshIon Channels - Physiologyen_US
dc.subject.meshMast Cells - Metabolismen_US
dc.subject.meshMuscle, Smooth - Physiopathologyen_US
dc.subject.meshNifedipine - Therapeutic Useen_US
dc.subject.meshPhysical Exertionen_US
dc.subject.meshSheepen_US
dc.subject.meshVerapamil - Therapeutic Useen_US
dc.titleCalcium channel blockers and asthmaen_US
dc.typeArticleen_US
dc.identifier.emailIp, M:msmip@hku.hken_US
dc.identifier.authorityIp, M=rp00347en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/BF02713625-
dc.identifier.pmid2419708-
dc.identifier.scopuseid_2-s2.0-0022641947en_US
dc.identifier.volume164en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage16en_US
dc.identifier.isiWOS:A1986AYL3000001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSo, SY=7102397816en_US
dc.identifier.scopusauthoridIp, M=7102423259en_US
dc.identifier.scopusauthoridLam, WK=7203021937en_US

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