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Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart
Adenosine‐5′‐triphosphate (ATP) and adenosine are potent coronary vasodilators. ATP is rapidly converted to adenosine by ectonucleotidases. We examined whether coronary vasodilation caused by exogenous ATP is mediated by P2 receptor activation or by A2A‐adenosine receptor activation. Effects of inte...
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| Published in: | British journal of pharmacology 2000-07, Vol.130 (5), p.1065-1075 |
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| container_title | British journal of pharmacology |
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| creator | Erga, Knut Ståle Seubert, Christoph N Liang, Hui‐Xiu Wu, Lin Shryock, John C Belardinelli, Luiz |
| description | Adenosine‐5′‐triphosphate (ATP) and adenosine are potent coronary vasodilators. ATP is rapidly converted to adenosine by ectonucleotidases. We examined whether coronary vasodilation caused by exogenous ATP is mediated by P2 receptor activation or by A2A‐adenosine receptor activation.
Effects of interventions on coronary conductance were determined by measuring coronary perfusion pressure in guinea‐pig isolated hearts perfused at a constant flow of 10 ml min−1.
ATP and adenosine both caused sustained, concentration‐dependent increases of coronary conductance. Maximal responses to both agonists were equivalent. The values of pD2 (±s.e.mean) for ATP and adenosine were 6.68±0.04 and 7.06±0.05, respectively. Adenosine was significantly more potent than ATP (P |
| doi_str_mv | 10.1038/sj.bjp.0703386 |
| format | article |
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Effects of interventions on coronary conductance were determined by measuring coronary perfusion pressure in guinea‐pig isolated hearts perfused at a constant flow of 10 ml min−1.
ATP and adenosine both caused sustained, concentration‐dependent increases of coronary conductance. Maximal responses to both agonists were equivalent. The values of pD2 (±s.e.mean) for ATP and adenosine were 6.68±0.04 and 7.06±0.05, respectively. Adenosine was significantly more potent than ATP (P<0.0001, n=10).
The values of pIC50 for the selective A2A‐adenosine receptor antagonist SCH58261 to antagonize equivalent responses to ATP and adenosine were 8.28±0.08 and 8.28±0.06 (P=0.99, n=6), respectively.
The non‐selective adenosine receptor antagonists xanthine amine congener (XAC) and CGS15943 antagonized similarly the equivalent vasodilations caused by ATP (pIC50 values 7.48±0.04 and 7.45±0.06, respectively) and adenosine (pIC50 values 7.37±0.13 and 7.56±0.11).
In contrast to ATP and adenosine, the two P2 agonists 2‐methylthio‐ATP and uridine‐5′‐triphosphate failed to cause stable increases of coronary conductance, caused desensitization of vasodilator responses, and were not antagonized by SCH 58261, 8‐parasulphophenyltheophylline, or XAC.
Glibenclamide attenuated coronary vasodilations caused by ATP and adenosine by 88 and 89%, respectively, but failed to attenuate those caused by 2‐methylthio‐ATP.
These results strongly suggest that sustained, submaximal coronary vasodilation caused by exogenous ATP is entirely mediated by adenosine acting upon A2A‐adenosine receptors.
British Journal of Pharmacology (2000) 130, 1065–1075; doi:10.1038/sj.bjp.0703386</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0703386</identifier><identifier>PMID: 10882391</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>A2A‐receptors ; adenosine ; Adenosinic and purinergic receptors ; AOPCP ; ARL67156 ; ATP ; Biological and medical sciences ; Cell receptors ; Cell structures and functions ; coronary regulation ; Fundamental and applied biological sciences. Psychology ; Isolated heart ; Molecular and cellular biology ; P2‐agonists ; vasodilation</subject><ispartof>British journal of pharmacology, 2000-07, Vol.130 (5), p.1065-1075</ispartof><rights>2000 British Pharmacological Society</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2000</rights><rights>Copyright 2000, Nature Publishing Group 2000 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1572153/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1572153/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1446496$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Erga, Knut Ståle</creatorcontrib><creatorcontrib>Seubert, Christoph N</creatorcontrib><creatorcontrib>Liang, Hui‐Xiu</creatorcontrib><creatorcontrib>Wu, Lin</creatorcontrib><creatorcontrib>Shryock, John C</creatorcontrib><creatorcontrib>Belardinelli, Luiz</creatorcontrib><title>Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart</title><title>British journal of pharmacology</title><description>Adenosine‐5′‐triphosphate (ATP) and adenosine are potent coronary vasodilators. ATP is rapidly converted to adenosine by ectonucleotidases. We examined whether coronary vasodilation caused by exogenous ATP is mediated by P2 receptor activation or by A2A‐adenosine receptor activation.
Effects of interventions on coronary conductance were determined by measuring coronary perfusion pressure in guinea‐pig isolated hearts perfused at a constant flow of 10 ml min−1.
ATP and adenosine both caused sustained, concentration‐dependent increases of coronary conductance. Maximal responses to both agonists were equivalent. The values of pD2 (±s.e.mean) for ATP and adenosine were 6.68±0.04 and 7.06±0.05, respectively. Adenosine was significantly more potent than ATP (P<0.0001, n=10).
The values of pIC50 for the selective A2A‐adenosine receptor antagonist SCH58261 to antagonize equivalent responses to ATP and adenosine were 8.28±0.08 and 8.28±0.06 (P=0.99, n=6), respectively.
The non‐selective adenosine receptor antagonists xanthine amine congener (XAC) and CGS15943 antagonized similarly the equivalent vasodilations caused by ATP (pIC50 values 7.48±0.04 and 7.45±0.06, respectively) and adenosine (pIC50 values 7.37±0.13 and 7.56±0.11).
In contrast to ATP and adenosine, the two P2 agonists 2‐methylthio‐ATP and uridine‐5′‐triphosphate failed to cause stable increases of coronary conductance, caused desensitization of vasodilator responses, and were not antagonized by SCH 58261, 8‐parasulphophenyltheophylline, or XAC.
Glibenclamide attenuated coronary vasodilations caused by ATP and adenosine by 88 and 89%, respectively, but failed to attenuate those caused by 2‐methylthio‐ATP.
These results strongly suggest that sustained, submaximal coronary vasodilation caused by exogenous ATP is entirely mediated by adenosine acting upon A2A‐adenosine receptors.
British Journal of Pharmacology (2000) 130, 1065–1075; doi:10.1038/sj.bjp.0703386</description><subject>A2A‐receptors</subject><subject>adenosine</subject><subject>Adenosinic and purinergic receptors</subject><subject>AOPCP</subject><subject>ARL67156</subject><subject>ATP</subject><subject>Biological and medical sciences</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>coronary regulation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Isolated heart</subject><subject>Molecular and cellular biology</subject><subject>P2‐agonists</subject><subject>vasodilation</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNpVkcFu1DAURS1ERYfClrWF2GZ4L05sZ4M0VECRKrVCZW05ycvUUWoHOzNVd3wC38iXYJgRVVfW0z06vtJl7A3CGkHo92lct-O8BgVCaPmMrbBSsqiFxudsBQCqQNT6lL1MaQTIoapfsFMErUvR4Iqlb2EiHga-KTe_f_6yPfmQnCceqaN5CZHbbnF7u7jg-ZDPzc115u6od3ahnnchBm_jA9_bFHo3HUDn-XaXLTajs9tyl8L0D78lG5dX7GSwU6LXx_eMff_86eb8ori8-vL1fHNZzNjUVaFET6ps7QAaq3qAtrRDQwpIiq4RQnS6IakFtbqVFrREJbDuFbQKJcBQijP24eCdd20u3JFfop3MHN1dbmyCdeZp4t2t2Ya9wVqVWIsseHsUxPBjR2kxY9hFnzubEhUqqRVm6N0Rsqmz0xCt71z6_wtWlawamTFxwO7dRA-PMZi_O5o0mryjOe5oPl5fYNVU4g_PfpYm</recordid><startdate>200007</startdate><enddate>200007</enddate><creator>Erga, Knut Ståle</creator><creator>Seubert, Christoph N</creator><creator>Liang, Hui‐Xiu</creator><creator>Wu, Lin</creator><creator>Shryock, John C</creator><creator>Belardinelli, Luiz</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>200007</creationdate><title>Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart</title><author>Erga, Knut Ståle ; Seubert, Christoph N ; Liang, Hui‐Xiu ; Wu, Lin ; Shryock, John C ; Belardinelli, Luiz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1954-73de72baf08145f0b2af9e70e63c9333c89e683eb8b6a08617315d70b71600f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>A2A‐receptors</topic><topic>adenosine</topic><topic>Adenosinic and purinergic receptors</topic><topic>AOPCP</topic><topic>ARL67156</topic><topic>ATP</topic><topic>Biological and medical sciences</topic><topic>Cell receptors</topic><topic>Cell structures and functions</topic><topic>coronary regulation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Isolated heart</topic><topic>Molecular and cellular biology</topic><topic>P2‐agonists</topic><topic>vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Erga, Knut Ståle</creatorcontrib><creatorcontrib>Seubert, Christoph N</creatorcontrib><creatorcontrib>Liang, Hui‐Xiu</creatorcontrib><creatorcontrib>Wu, Lin</creatorcontrib><creatorcontrib>Shryock, John C</creatorcontrib><creatorcontrib>Belardinelli, Luiz</creatorcontrib><collection>Pascal-Francis</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Biological Science Journals</collection><collection>Nursing & Allied Health Premium</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>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Erga, Knut Ståle</au><au>Seubert, Christoph N</au><au>Liang, Hui‐Xiu</au><au>Wu, Lin</au><au>Shryock, John C</au><au>Belardinelli, Luiz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart</atitle><jtitle>British journal of pharmacology</jtitle><date>2000-07</date><risdate>2000</risdate><volume>130</volume><issue>5</issue><spage>1065</spage><epage>1075</epage><pages>1065-1075</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Adenosine‐5′‐triphosphate (ATP) and adenosine are potent coronary vasodilators. ATP is rapidly converted to adenosine by ectonucleotidases. We examined whether coronary vasodilation caused by exogenous ATP is mediated by P2 receptor activation or by A2A‐adenosine receptor activation.
Effects of interventions on coronary conductance were determined by measuring coronary perfusion pressure in guinea‐pig isolated hearts perfused at a constant flow of 10 ml min−1.
ATP and adenosine both caused sustained, concentration‐dependent increases of coronary conductance. Maximal responses to both agonists were equivalent. The values of pD2 (±s.e.mean) for ATP and adenosine were 6.68±0.04 and 7.06±0.05, respectively. Adenosine was significantly more potent than ATP (P<0.0001, n=10).
The values of pIC50 for the selective A2A‐adenosine receptor antagonist SCH58261 to antagonize equivalent responses to ATP and adenosine were 8.28±0.08 and 8.28±0.06 (P=0.99, n=6), respectively.
The non‐selective adenosine receptor antagonists xanthine amine congener (XAC) and CGS15943 antagonized similarly the equivalent vasodilations caused by ATP (pIC50 values 7.48±0.04 and 7.45±0.06, respectively) and adenosine (pIC50 values 7.37±0.13 and 7.56±0.11).
In contrast to ATP and adenosine, the two P2 agonists 2‐methylthio‐ATP and uridine‐5′‐triphosphate failed to cause stable increases of coronary conductance, caused desensitization of vasodilator responses, and were not antagonized by SCH 58261, 8‐parasulphophenyltheophylline, or XAC.
Glibenclamide attenuated coronary vasodilations caused by ATP and adenosine by 88 and 89%, respectively, but failed to attenuate those caused by 2‐methylthio‐ATP.
These results strongly suggest that sustained, submaximal coronary vasodilation caused by exogenous ATP is entirely mediated by adenosine acting upon A2A‐adenosine receptors.
British Journal of Pharmacology (2000) 130, 1065–1075; doi:10.1038/sj.bjp.0703386</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10882391</pmid><doi>10.1038/sj.bjp.0703386</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | A2A‐receptors adenosine Adenosinic and purinergic receptors AOPCP ARL67156 ATP Biological and medical sciences Cell receptors Cell structures and functions coronary regulation Fundamental and applied biological sciences. Psychology Isolated heart Molecular and cellular biology P2‐agonists vasodilation |
| title | Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart |
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