Pertussis toxin unmasks stimulatory myocardial A2-adenosine receptors on ventricular cardiomyocytes
Pertussis toxin-pretreatment abolished the contractility- and cAMP-decreasing effects of the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (R-PIA) in the presence of isoprenaline in isolated ventricular cardiomyocytes from guinea-pigs, indicating that these stimulatory effects of A1-...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 1993-06, Vol.25 (6), p.655-659 |
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| container_title | Journal of molecular and cellular cardiology |
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| creator | STEIN, B MENDE, U NEUMANN, J SCHMITZ, W SCHOLZ, H |
| description | Pertussis toxin-pretreatment abolished the contractility- and cAMP-decreasing effects of the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (R-PIA) in the presence of isoprenaline in isolated ventricular cardiomyocytes from guinea-pigs, indicating that these stimulatory effects of A1-adenosine receptors are mediated via pertussis toxin-sensitive G-proteins. Furthermore, the decrease in contractile response by the A1/A2-adenosine receptor agonist 5'-N-ethylcarboxamidadenosine (NECA) was abolished. Moreover, NECA increased cAMP content in pertussis toxin-pretreated cells. Thus, pertussis toxin unmasked cAMP-augmenting effects of NECA, indicating that NECA can stimulate A2-adenosine receptors on cardiomyocytes. Thereby, the present study provides evidence that besides cAMP- and contractility-decreasing A1-adenosine receptors, cAMP-increasing A2-adenosine receptors coexist on ventricular cardiomyocytes, which do not influence contractile response. |
| doi_str_mv | 10.1006/jmcc.1993.1078 |
| format | Article |
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Furthermore, the decrease in contractile response by the A1/A2-adenosine receptor agonist 5'-N-ethylcarboxamidadenosine (NECA) was abolished. Moreover, NECA increased cAMP content in pertussis toxin-pretreated cells. Thus, pertussis toxin unmasked cAMP-augmenting effects of NECA, indicating that NECA can stimulate A2-adenosine receptors on cardiomyocytes. Thereby, the present study provides evidence that besides cAMP- and contractility-decreasing A1-adenosine receptors, cAMP-increasing A2-adenosine receptors coexist on ventricular cardiomyocytes, which do not influence contractile response.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1006/jmcc.1993.1078</identifier><identifier>PMID: 8411191</identifier><identifier>CODEN: JMCDAY</identifier><language>eng</language><publisher>Kent: Elsevier</publisher><subject>Adenosine - analogs & derivatives ; Adenosine - pharmacology ; Adenosine-5'-(N-ethylcarboxamide) ; Adenosinic and purinergic receptors ; Animals ; Biological and medical sciences ; Cell receptors ; Cell structures and functions ; Cyclic AMP - analysis ; Fundamental and applied biological sciences. Psychology ; GTP-Binding Proteins - physiology ; Guinea Pigs ; Heart Ventricles - chemistry ; Heart Ventricles - cytology ; Heart Ventricles - ultrastructure ; Isoproterenol - pharmacology ; Molecular and cellular biology ; Myocardial Contraction - physiology ; Myocardium - chemistry ; Myocardium - cytology ; Myocardium - ultrastructure ; Pertussis Toxin ; Phenylisopropyladenosine - pharmacology ; Receptors, Purinergic P1 - analysis ; Receptors, Purinergic P1 - drug effects ; Receptors, Purinergic P1 - physiology ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Vasodilator Agents - pharmacology ; Virulence Factors, Bordetella - pharmacology</subject><ispartof>Journal of molecular and cellular cardiology, 1993-06, Vol.25 (6), p.655-659</ispartof><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c234t-8eb751e3df44000b6049c66485e35096160575706a9982bf28c42492876cbc1d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3759296$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8411191$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>STEIN, B</creatorcontrib><creatorcontrib>MENDE, U</creatorcontrib><creatorcontrib>NEUMANN, J</creatorcontrib><creatorcontrib>SCHMITZ, W</creatorcontrib><creatorcontrib>SCHOLZ, H</creatorcontrib><title>Pertussis toxin unmasks stimulatory myocardial A2-adenosine receptors on ventricular cardiomyocytes</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>Pertussis toxin-pretreatment abolished the contractility- and cAMP-decreasing effects of the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (R-PIA) in the presence of isoprenaline in isolated ventricular cardiomyocytes from guinea-pigs, indicating that these stimulatory effects of A1-adenosine receptors are mediated via pertussis toxin-sensitive G-proteins. Furthermore, the decrease in contractile response by the A1/A2-adenosine receptor agonist 5'-N-ethylcarboxamidadenosine (NECA) was abolished. Moreover, NECA increased cAMP content in pertussis toxin-pretreated cells. Thus, pertussis toxin unmasked cAMP-augmenting effects of NECA, indicating that NECA can stimulate A2-adenosine receptors on cardiomyocytes. Thereby, the present study provides evidence that besides cAMP- and contractility-decreasing A1-adenosine receptors, cAMP-increasing A2-adenosine receptors coexist on ventricular cardiomyocytes, which do not influence contractile response.</description><subject>Adenosine - analogs & derivatives</subject><subject>Adenosine - pharmacology</subject><subject>Adenosine-5'-(N-ethylcarboxamide)</subject><subject>Adenosinic and purinergic receptors</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>Cyclic AMP - analysis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GTP-Binding Proteins - physiology</subject><subject>Guinea Pigs</subject><subject>Heart Ventricles - chemistry</subject><subject>Heart Ventricles - cytology</subject><subject>Heart Ventricles - ultrastructure</subject><subject>Isoproterenol - pharmacology</subject><subject>Molecular and cellular biology</subject><subject>Myocardial Contraction - physiology</subject><subject>Myocardium - chemistry</subject><subject>Myocardium - cytology</subject><subject>Myocardium - ultrastructure</subject><subject>Pertussis Toxin</subject><subject>Phenylisopropyladenosine - pharmacology</subject><subject>Receptors, Purinergic P1 - analysis</subject><subject>Receptors, Purinergic P1 - drug effects</subject><subject>Receptors, Purinergic P1 - physiology</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Virulence Factors, Bordetella - pharmacology</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1Lw0AQhhdRaq1evQl7EG-p-53dYxG_oKAHPYfNZgNbk2zdScT-exNbehqGed6X4UHompIlJUTdb1rnltQYPq65PkFzSozMtNTiFM0JYSxjmulzdAGwIYQYwfkMzbSglBo6R-7dp34ACID7-Bs6PHSthS_A0Id2aGwf0w63u-hsqoJt8IpltvJdhNB5nLzz25EAHDv847s-BTdmEv6n4xTb9R4u0VltG_BXh7lAn0-PHw8v2frt-fVhtc4c46LPtC9zST2vaiHGT0tFhHFKCS09l8QoqojMZU6UNUazsmbaCSYM07lypaMVX6C7fe82xe_BQ1-0AZxvGtv5OECRq7E2l2oEl3vQpQiQfF1sU2ht2hWUFJPVYrJaTFaLyeoYuDk0D2XrqyN-0Djebw93C842dbKdC3DEeC4NM4r_AfRcgRw</recordid><startdate>199306</startdate><enddate>199306</enddate><creator>STEIN, B</creator><creator>MENDE, U</creator><creator>NEUMANN, J</creator><creator>SCHMITZ, W</creator><creator>SCHOLZ, H</creator><general>Elsevier</general><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>7X8</scope></search><sort><creationdate>199306</creationdate><title>Pertussis toxin unmasks stimulatory myocardial A2-adenosine receptors on ventricular cardiomyocytes</title><author>STEIN, B ; MENDE, U ; NEUMANN, J ; SCHMITZ, W ; SCHOLZ, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c234t-8eb751e3df44000b6049c66485e35096160575706a9982bf28c42492876cbc1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adenosine - analogs & derivatives</topic><topic>Adenosine - pharmacology</topic><topic>Adenosine-5'-(N-ethylcarboxamide)</topic><topic>Adenosinic and purinergic receptors</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell receptors</topic><topic>Cell structures and functions</topic><topic>Cyclic AMP - analysis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GTP-Binding Proteins - physiology</topic><topic>Guinea Pigs</topic><topic>Heart Ventricles - chemistry</topic><topic>Heart Ventricles - cytology</topic><topic>Heart Ventricles - ultrastructure</topic><topic>Isoproterenol - pharmacology</topic><topic>Molecular and cellular biology</topic><topic>Myocardial Contraction - physiology</topic><topic>Myocardium - chemistry</topic><topic>Myocardium - cytology</topic><topic>Myocardium - ultrastructure</topic><topic>Pertussis Toxin</topic><topic>Phenylisopropyladenosine - pharmacology</topic><topic>Receptors, Purinergic P1 - analysis</topic><topic>Receptors, Purinergic P1 - drug effects</topic><topic>Receptors, Purinergic P1 - physiology</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Virulence Factors, Bordetella - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>STEIN, B</creatorcontrib><creatorcontrib>MENDE, U</creatorcontrib><creatorcontrib>NEUMANN, J</creatorcontrib><creatorcontrib>SCHMITZ, W</creatorcontrib><creatorcontrib>SCHOLZ, H</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>STEIN, B</au><au>MENDE, U</au><au>NEUMANN, J</au><au>SCHMITZ, W</au><au>SCHOLZ, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pertussis toxin unmasks stimulatory myocardial A2-adenosine receptors on ventricular cardiomyocytes</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>1993-06</date><risdate>1993</risdate><volume>25</volume><issue>6</issue><spage>655</spage><epage>659</epage><pages>655-659</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><coden>JMCDAY</coden><abstract>Pertussis toxin-pretreatment abolished the contractility- and cAMP-decreasing effects of the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (R-PIA) in the presence of isoprenaline in isolated ventricular cardiomyocytes from guinea-pigs, indicating that these stimulatory effects of A1-adenosine receptors are mediated via pertussis toxin-sensitive G-proteins. Furthermore, the decrease in contractile response by the A1/A2-adenosine receptor agonist 5'-N-ethylcarboxamidadenosine (NECA) was abolished. Moreover, NECA increased cAMP content in pertussis toxin-pretreated cells. Thus, pertussis toxin unmasked cAMP-augmenting effects of NECA, indicating that NECA can stimulate A2-adenosine receptors on cardiomyocytes. Thereby, the present study provides evidence that besides cAMP- and contractility-decreasing A1-adenosine receptors, cAMP-increasing A2-adenosine receptors coexist on ventricular cardiomyocytes, which do not influence contractile response.</abstract><cop>Kent</cop><pub>Elsevier</pub><pmid>8411191</pmid><doi>10.1006/jmcc.1993.1078</doi><tpages>5</tpages></addata></record> |
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| subjects | Adenosine - analogs & derivatives Adenosine - pharmacology Adenosine-5'-(N-ethylcarboxamide) Adenosinic and purinergic receptors Animals Biological and medical sciences Cell receptors Cell structures and functions Cyclic AMP - analysis Fundamental and applied biological sciences. Psychology GTP-Binding Proteins - physiology Guinea Pigs Heart Ventricles - chemistry Heart Ventricles - cytology Heart Ventricles - ultrastructure Isoproterenol - pharmacology Molecular and cellular biology Myocardial Contraction - physiology Myocardium - chemistry Myocardium - cytology Myocardium - ultrastructure Pertussis Toxin Phenylisopropyladenosine - pharmacology Receptors, Purinergic P1 - analysis Receptors, Purinergic P1 - drug effects Receptors, Purinergic P1 - physiology Signal Transduction - drug effects Signal Transduction - physiology Vasodilator Agents - pharmacology Virulence Factors, Bordetella - pharmacology |
| title | Pertussis toxin unmasks stimulatory myocardial A2-adenosine receptors on ventricular cardiomyocytes |
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