Role of cysteinyl leukotrienes in adenosine 5`-monophosphate induced bronchoconstriction in asthma
Background: Adenosine induced bronchoconstriction in patients with asthma is thought to be mediated by the synthesis and release of autacoids from airway mast cells. In vitro, adenosine induced constriction of asthmatic bronchi is blocked by a combination of specific histamine and cysteinyl leukotri...
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description | Background: Adenosine induced bronchoconstriction in patients with asthma is thought to be mediated by the synthesis and release of autacoids from airway mast cells. In vitro, adenosine induced constriction of asthmatic bronchi is blocked by a combination of specific histamine and cysteinyl leukotriene receptor antagonists, but the relative contribution of these mediators in vivo is unclear. We hypothesised that adenosine induced bronchoconstriction in asthmatic patients may be blocked by pretreatment with the orally active selective cysteinyl leukotriene-1 (CysLT1) receptor antagonist, montelukast. Methods: In a randomised, double blind, crossover study, oral montelukast (10 mg) or placebo was administered once daily on two consecutive days to 18 patients with mild to moderate persistent atopic asthma. Incremental doses of adenosine 5`-monophosphate (AMP) from 0.39 to 400 mg/ml were inhaled by dosimeter and the dose producing a 20% fall in FEV1 (PC20AMP) after AMP inhalation was recorded. Leukotriene E4 (LTE4) urinary concentrations were measured by enzyme immunoassay 4 hours after AMP challenge. Results: Montelukast pretreatment provided highly significant protection against adenosine induced bronchoconstriction, with geometric mean PC20AMP values of 52.6 mg/ml (95% CI 35.2 to 78.7) after placebo and 123.9 mg/ml (95% CI 83.0 to 185.0) after montelukast (p=0.006). The geometric mean of the montelukast/placebo PC20AMP ratio was 2.4 (95% CI 1.3 to 4.2). Montelukast had no significant effect on 4 hour urinary excretion of LTE4 compared with placebo. Conclusions: Selective CysLT1 receptor antagonism with montelukast provides highly significant protection against AMP induced bronchoconstriction in patients with atopic asthma, implying that cysteinyl leukotrienes are generated from airway mast cells through preferential activation of their A2B receptors. |
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In vitro, adenosine induced constriction of asthmatic bronchi is blocked by a combination of specific histamine and cysteinyl leukotriene receptor antagonists, but the relative contribution of these mediators in vivo is unclear. We hypothesised that adenosine induced bronchoconstriction in asthmatic patients may be blocked by pretreatment with the orally active selective cysteinyl leukotriene-1 (CysLT1) receptor antagonist, montelukast. Methods: In a randomised, double blind, crossover study, oral montelukast (10 mg) or placebo was administered once daily on two consecutive days to 18 patients with mild to moderate persistent atopic asthma. Incremental doses of adenosine 5`-monophosphate (AMP) from 0.39 to 400 mg/ml were inhaled by dosimeter and the dose producing a 20% fall in FEV1 (PC20AMP) after AMP inhalation was recorded. Leukotriene E4 (LTE4) urinary concentrations were measured by enzyme immunoassay 4 hours after AMP challenge. Results: Montelukast pretreatment provided highly significant protection against adenosine induced bronchoconstriction, with geometric mean PC20AMP values of 52.6 mg/ml (95% CI 35.2 to 78.7) after placebo and 123.9 mg/ml (95% CI 83.0 to 185.0) after montelukast (p=0.006). The geometric mean of the montelukast/placebo PC20AMP ratio was 2.4 (95% CI 1.3 to 4.2). Montelukast had no significant effect on 4 hour urinary excretion of LTE4 compared with placebo. Conclusions: Selective CysLT1 receptor antagonism with montelukast provides highly significant protection against AMP induced bronchoconstriction in patients with atopic asthma, implying that cysteinyl leukotrienes are generated from airway mast cells through preferential activation of their A2B receptors.</description><identifier>ISSN: 0040-6376</identifier><identifier>EISSN: 1468-3296</identifier><identifier>DOI: 10.1136/thorax.57.4.323</identifier><identifier>PMID: 11923550</identifier><identifier>CODEN: THORA7</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Thoracic Society</publisher><subject>Acetates - therapeutic use ; Adenosine ; adenosine induced bronchoconstriction ; Adenosine Monophosphate - administration & dosage ; Adenosine Monophosphate - adverse effects ; Adult ; Allergic diseases ; Anti-Asthmatic Agents - therapeutic use ; Asthma ; Asthma - drug therapy ; Asthma - physiopathology ; Asthma - urine ; Biological and medical sciences ; Bronchial spasm ; Bronchoconstriction - drug effects ; Cross-Over Studies ; cysteinyl leukotrienes ; Double-Blind Method ; Drug therapy ; Female ; Forced Expiratory Volume - physiology ; Histamine ; Humans ; Immunopathology ; Leukotriene Antagonists - therapeutic use ; Leukotriene E4 - urine ; Leukotrienes ; Male ; Medical sciences ; Membrane Proteins ; Middle Aged ; montelukast ; Original ; Physiological aspects ; Quinolines - therapeutic use ; Receptors, Leukotriene ; Respiratory and ent allergic diseases ; Synthesis</subject><ispartof>Thorax, 2002-04, Vol.57 (4), p.323-327</ispartof><rights>Copyright 2002 Thorax</rights><rights>2002 INIST-CNRS</rights><rights>COPYRIGHT 2002 BMJ Publishing Group Ltd.</rights><rights>Copyright: 2002 Copyright 2002 Thorax</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b595t-379c4db7806452e46f10a3384f22752ac488d3f24d70294f282460e54d77fcb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1746289/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1746289/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13584657$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11923550$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rorke, S</creatorcontrib><creatorcontrib>Jennison, S</creatorcontrib><creatorcontrib>Jeffs, J A</creatorcontrib><creatorcontrib>Sampson, A P</creatorcontrib><creatorcontrib>Arshad, H</creatorcontrib><creatorcontrib>Holgate, S T</creatorcontrib><title>Role of cysteinyl leukotrienes in adenosine 5`-monophosphate induced bronchoconstriction in asthma</title><title>Thorax</title><addtitle>Thorax</addtitle><description>Background: Adenosine induced bronchoconstriction in patients with asthma is thought to be mediated by the synthesis and release of autacoids from airway mast cells. In vitro, adenosine induced constriction of asthmatic bronchi is blocked by a combination of specific histamine and cysteinyl leukotriene receptor antagonists, but the relative contribution of these mediators in vivo is unclear. We hypothesised that adenosine induced bronchoconstriction in asthmatic patients may be blocked by pretreatment with the orally active selective cysteinyl leukotriene-1 (CysLT1) receptor antagonist, montelukast. Methods: In a randomised, double blind, crossover study, oral montelukast (10 mg) or placebo was administered once daily on two consecutive days to 18 patients with mild to moderate persistent atopic asthma. Incremental doses of adenosine 5`-monophosphate (AMP) from 0.39 to 400 mg/ml were inhaled by dosimeter and the dose producing a 20% fall in FEV1 (PC20AMP) after AMP inhalation was recorded. Leukotriene E4 (LTE4) urinary concentrations were measured by enzyme immunoassay 4 hours after AMP challenge. Results: Montelukast pretreatment provided highly significant protection against adenosine induced bronchoconstriction, with geometric mean PC20AMP values of 52.6 mg/ml (95% CI 35.2 to 78.7) after placebo and 123.9 mg/ml (95% CI 83.0 to 185.0) after montelukast (p=0.006). The geometric mean of the montelukast/placebo PC20AMP ratio was 2.4 (95% CI 1.3 to 4.2). Montelukast had no significant effect on 4 hour urinary excretion of LTE4 compared with placebo. Conclusions: Selective CysLT1 receptor antagonism with montelukast provides highly significant protection against AMP induced bronchoconstriction in patients with atopic asthma, implying that cysteinyl leukotrienes are generated from airway mast cells through preferential activation of their A2B receptors.</description><subject>Acetates - therapeutic use</subject><subject>Adenosine</subject><subject>adenosine induced bronchoconstriction</subject><subject>Adenosine Monophosphate - administration & dosage</subject><subject>Adenosine Monophosphate - adverse effects</subject><subject>Adult</subject><subject>Allergic diseases</subject><subject>Anti-Asthmatic Agents - therapeutic use</subject><subject>Asthma</subject><subject>Asthma - drug therapy</subject><subject>Asthma - physiopathology</subject><subject>Asthma - urine</subject><subject>Biological and medical sciences</subject><subject>Bronchial spasm</subject><subject>Bronchoconstriction - drug effects</subject><subject>Cross-Over Studies</subject><subject>cysteinyl leukotrienes</subject><subject>Double-Blind Method</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Forced Expiratory Volume - physiology</subject><subject>Histamine</subject><subject>Humans</subject><subject>Immunopathology</subject><subject>Leukotriene Antagonists - therapeutic use</subject><subject>Leukotriene E4 - urine</subject><subject>Leukotrienes</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins</subject><subject>Middle Aged</subject><subject>montelukast</subject><subject>Original</subject><subject>Physiological aspects</subject><subject>Quinolines - therapeutic use</subject><subject>Receptors, Leukotriene</subject><subject>Respiratory and ent allergic diseases</subject><subject>Synthesis</subject><issn>0040-6376</issn><issn>1468-3296</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkt9rFDEQx4Mo9qw--yYL4ou41_xO9kUoh1rhqLQUfYzZbPY2193kTHal998b3aOnUJA8hMx85svMfAPASwSXCBF-NnYh6rslE0u6JJg8AgtEuSwJrvhjsICQwpITwU_As5S2EEKJkHgKThCqMGEMLkB9HXpbhLYw-zRa5_d90dvpNozRWW9T4XyhG-tDct4W7Hs5BB92XUi7To82Z5vJ2KaoY_CmCyb4lAvN6IL_U5nGbtDPwZNW98m-ONyn4Objh5vVRbn-8unz6nxd1qxiY0lEZWhTCwk5ZdhS3iKoCZG0xVgwrA2VsiEtpo2AuMpRiSmHluW3aE1NTsH7WXY31YNtjPVj1L3aRTfouFdBO_VvxrtObcJPhQTlWFZZ4PVBIIYfk02j2oYp-txyRiSSkMgKZurdTG10b5XzbV6VNpu8rKwZvG1dDp9LJvK2mcx4-QCeT2MHZx7iz2bexJBStO39AAiq35ar2XLFhKIqW54rXv0995E_eJyBNwdAJ6P7NmpvXDpyhEnKmTi26vJPuLvP63iruCCCqcuvK7W-XF99u7haqevMv535etj-t8tfKAPUTA</recordid><startdate>20020401</startdate><enddate>20020401</enddate><creator>Rorke, S</creator><creator>Jennison, S</creator><creator>Jeffs, J A</creator><creator>Sampson, A P</creator><creator>Arshad, H</creator><creator>Holgate, S T</creator><general>BMJ Publishing Group Ltd and British Thoracic Society</general><general>BMJ</general><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><general>BMJ Group</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20020401</creationdate><title>Role of cysteinyl leukotrienes in adenosine 5`-monophosphate induced bronchoconstriction in asthma</title><author>Rorke, S ; Jennison, S ; Jeffs, J A ; Sampson, A P ; Arshad, H ; Holgate, S T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b595t-379c4db7806452e46f10a3384f22752ac488d3f24d70294f282460e54d77fcb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acetates - therapeutic use</topic><topic>Adenosine</topic><topic>adenosine induced bronchoconstriction</topic><topic>Adenosine Monophosphate - administration & dosage</topic><topic>Adenosine Monophosphate - adverse effects</topic><topic>Adult</topic><topic>Allergic diseases</topic><topic>Anti-Asthmatic Agents - therapeutic use</topic><topic>Asthma</topic><topic>Asthma - drug therapy</topic><topic>Asthma - physiopathology</topic><topic>Asthma - urine</topic><topic>Biological and medical sciences</topic><topic>Bronchial spasm</topic><topic>Bronchoconstriction - drug effects</topic><topic>Cross-Over Studies</topic><topic>cysteinyl leukotrienes</topic><topic>Double-Blind Method</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Forced Expiratory Volume - physiology</topic><topic>Histamine</topic><topic>Humans</topic><topic>Immunopathology</topic><topic>Leukotriene Antagonists - therapeutic use</topic><topic>Leukotriene E4 - urine</topic><topic>Leukotrienes</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins</topic><topic>Middle Aged</topic><topic>montelukast</topic><topic>Original</topic><topic>Physiological aspects</topic><topic>Quinolines - therapeutic use</topic><topic>Receptors, Leukotriene</topic><topic>Respiratory and ent allergic diseases</topic><topic>Synthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rorke, S</creatorcontrib><creatorcontrib>Jennison, S</creatorcontrib><creatorcontrib>Jeffs, J A</creatorcontrib><creatorcontrib>Sampson, A P</creatorcontrib><creatorcontrib>Arshad, H</creatorcontrib><creatorcontrib>Holgate, S T</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Thorax</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rorke, S</au><au>Jennison, S</au><au>Jeffs, J A</au><au>Sampson, A P</au><au>Arshad, H</au><au>Holgate, S T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of cysteinyl leukotrienes in adenosine 5`-monophosphate induced bronchoconstriction in asthma</atitle><jtitle>Thorax</jtitle><addtitle>Thorax</addtitle><date>2002-04-01</date><risdate>2002</risdate><volume>57</volume><issue>4</issue><spage>323</spage><epage>327</epage><pages>323-327</pages><issn>0040-6376</issn><eissn>1468-3296</eissn><coden>THORA7</coden><abstract>Background: Adenosine induced bronchoconstriction in patients with asthma is thought to be mediated by the synthesis and release of autacoids from airway mast cells. In vitro, adenosine induced constriction of asthmatic bronchi is blocked by a combination of specific histamine and cysteinyl leukotriene receptor antagonists, but the relative contribution of these mediators in vivo is unclear. We hypothesised that adenosine induced bronchoconstriction in asthmatic patients may be blocked by pretreatment with the orally active selective cysteinyl leukotriene-1 (CysLT1) receptor antagonist, montelukast. Methods: In a randomised, double blind, crossover study, oral montelukast (10 mg) or placebo was administered once daily on two consecutive days to 18 patients with mild to moderate persistent atopic asthma. Incremental doses of adenosine 5`-monophosphate (AMP) from 0.39 to 400 mg/ml were inhaled by dosimeter and the dose producing a 20% fall in FEV1 (PC20AMP) after AMP inhalation was recorded. Leukotriene E4 (LTE4) urinary concentrations were measured by enzyme immunoassay 4 hours after AMP challenge. Results: Montelukast pretreatment provided highly significant protection against adenosine induced bronchoconstriction, with geometric mean PC20AMP values of 52.6 mg/ml (95% CI 35.2 to 78.7) after placebo and 123.9 mg/ml (95% CI 83.0 to 185.0) after montelukast (p=0.006). The geometric mean of the montelukast/placebo PC20AMP ratio was 2.4 (95% CI 1.3 to 4.2). Montelukast had no significant effect on 4 hour urinary excretion of LTE4 compared with placebo. Conclusions: Selective CysLT1 receptor antagonism with montelukast provides highly significant protection against AMP induced bronchoconstriction in patients with atopic asthma, implying that cysteinyl leukotrienes are generated from airway mast cells through preferential activation of their A2B receptors.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Thoracic Society</pub><pmid>11923550</pmid><doi>10.1136/thorax.57.4.323</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acetates - therapeutic use Adenosine adenosine induced bronchoconstriction Adenosine Monophosphate - administration & dosage Adenosine Monophosphate - adverse effects Adult Allergic diseases Anti-Asthmatic Agents - therapeutic use Asthma Asthma - drug therapy Asthma - physiopathology Asthma - urine Biological and medical sciences Bronchial spasm Bronchoconstriction - drug effects Cross-Over Studies cysteinyl leukotrienes Double-Blind Method Drug therapy Female Forced Expiratory Volume - physiology Histamine Humans Immunopathology Leukotriene Antagonists - therapeutic use Leukotriene E4 - urine Leukotrienes Male Medical sciences Membrane Proteins Middle Aged montelukast Original Physiological aspects Quinolines - therapeutic use Receptors, Leukotriene Respiratory and ent allergic diseases Synthesis |
title | Role of cysteinyl leukotrienes in adenosine 5`-monophosphate induced bronchoconstriction in asthma |
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