In vitro and in vivo pharmacology of a structurally novel Na+‐H+ exchange inhibitor, T‐162559
We investigated the inhibitory effects of a non‐acylguanidine Na+‐H+ exchange (NHE) inhibitor, T‐162559 ((5E,7S)‐[7‐(5‐fluoro‐2‐methylphenyl)‐4‐methyl‐7,8‐dihydro‐5(6H)‐quinolinylideneamino] guanidine dimethanesulphonate), on NHE‐1, and its cardioprotective effect against ischaemia and reperfusion i...
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| Veröffentlicht in: | British journal of pharmacology 2002-04, Vol.135 (8), p.1995-2003 |
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| container_issue | 8 |
| container_start_page | 1995 |
| container_title | British journal of pharmacology |
| container_volume | 135 |
| creator | Kusumoto, Keiji Igata, Hideki Abe, Akemi Ikeda, Shota Tsuboi, Ayako Imamiya, Eikoh Fukumoto, Shoji Shiraishi, Mitsuru Watanabe, Toshifumi |
| description | We investigated the inhibitory effects of a non‐acylguanidine Na+‐H+ exchange (NHE) inhibitor, T‐162559 ((5E,7S)‐[7‐(5‐fluoro‐2‐methylphenyl)‐4‐methyl‐7,8‐dihydro‐5(6H)‐quinolinylideneamino] guanidine dimethanesulphonate), on NHE‐1, and its cardioprotective effect against ischaemia and reperfusion injury in rats and rabbits.
T‐162559 inhibited human platelet NHE‐1 in a concentration‐dependent manner, with an IC50 value of 13±3 nmol l−1, making it 16 and three times more potent than cariporide IC50: 209±75 nmol l−1, P |
| doi_str_mv | 10.1038/sj.bjp.0704647 |
| format | Article |
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T‐162559 inhibited human platelet NHE‐1 in a concentration‐dependent manner, with an IC50 value of 13±3 nmol l−1, making it 16 and three times more potent than cariporide IC50: 209±75 nmol l−1, P<0.01) and eniporide (IC50: 40±11 nmol l−1, P=0.066), respectively. T‐162559 also inhibited rat NHE‐1 with an IC50 value of 14±2 nmol l−1, which was five and three times lower than that of cariporide (IC50: 75±7 nmol l−1, P<0.01) and eniporide (IC50: 44±2 nmol l−1, P<0.01), respectively.
T‐162559 inhibited, in a concentration‐dependent manner, the reduction in cardiac contractility, progression of cardiac contracture, and increase in lactate dehydrogenase release after global ischaemia and reperfusion in perfused rat hearts. The inhibitory effects of T‐162559 were observed at a lower concentration range (10 – 100 nmol l−1) than with cariporide and eniporide. T‐162559 did not alter basal cardiac contractility or coronary flow after reperfusion, suggesting that it exerts direct cardioprotective effects on the heart.
Intravenous administration of T‐162559 (0.03 and 0.1 mg kg−1) significantly inhibited the progression of myocardial infarction induced by left coronary artery occlusion and reperfusion in rabbits; the infarct size normalized by area at risk was 74±6% in the vehicle group, and 47±5% and 51±7% in the T‐162559‐0.03 mg kg−1 and T‐162559‐0.1 mg kg−1 groups (both P<0.05), respectively.
These results indicate that the new structural NHE‐1 inhibitor T‐162559 is more potent than cariporide and eniporide and possesses a cardioprotective effect against ischaemia and reperfusion injury in rat and rabbit models.
British Journal of Pharmacology (2002) 135, 1995–2003; doi:10.1038/sj.bjp.0704647</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0704647</identifier><identifier>PMID: 11959803</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blood Platelets - drug effects ; Blood Platelets - metabolism ; cardioprotection ; Cardiotonic Agents - administration & dosage ; Cardiotonic Agents - pharmacology ; Cardiovascular system ; cariporide ; Dose-Response Relationship, Drug ; eniporide ; Guanidines - administration & dosage ; Guanidines - chemistry ; Guanidines - pharmacology ; Humans ; In Vitro Techniques ; Injections, Intravenous ; ischaemia‐reperfusion ; Male ; Medical sciences ; Miscellaneous ; myocardial infarction ; Myocardial Infarction - pathology ; Myocardial Infarction - prevention & control ; Myocardial Ischemia - drug therapy ; Myocardial Reperfusion Injury - drug therapy ; Na+‐H+ exchanger ; Pharmacology. Drug treatments ; Quinolines - administration & dosage ; Quinolines - chemistry ; Quinolines - pharmacology ; Rabbits ; Rats ; Rats, Wistar ; Sodium-Hydrogen Exchangers - antagonists & inhibitors ; Sulfones - pharmacology</subject><ispartof>British journal of pharmacology, 2002-04, Vol.135 (8), p.1995-2003</ispartof><rights>2002 British Pharmacological Society</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 2002</rights><rights>Copyright 2002, Nature Publishing Group 2002 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4878-138940841b466a1978607bbd14af85b5b7b2c47c42f7de0040def05d34a47f263</citedby><cites>FETCH-LOGICAL-c4878-138940841b466a1978607bbd14af85b5b7b2c47c42f7de0040def05d34a47f263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573312/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573312/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,27929,27930,45579,45580,46414,46838,53796,53798</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13684740$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11959803$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kusumoto, Keiji</creatorcontrib><creatorcontrib>Igata, Hideki</creatorcontrib><creatorcontrib>Abe, Akemi</creatorcontrib><creatorcontrib>Ikeda, Shota</creatorcontrib><creatorcontrib>Tsuboi, Ayako</creatorcontrib><creatorcontrib>Imamiya, Eikoh</creatorcontrib><creatorcontrib>Fukumoto, Shoji</creatorcontrib><creatorcontrib>Shiraishi, Mitsuru</creatorcontrib><creatorcontrib>Watanabe, Toshifumi</creatorcontrib><title>In vitro and in vivo pharmacology of a structurally novel Na+‐H+ exchange inhibitor, T‐162559</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>We investigated the inhibitory effects of a non‐acylguanidine Na+‐H+ exchange (NHE) inhibitor, T‐162559 ((5E,7S)‐[7‐(5‐fluoro‐2‐methylphenyl)‐4‐methyl‐7,8‐dihydro‐5(6H)‐quinolinylideneamino] guanidine dimethanesulphonate), on NHE‐1, and its cardioprotective effect against ischaemia and reperfusion injury in rats and rabbits.
T‐162559 inhibited human platelet NHE‐1 in a concentration‐dependent manner, with an IC50 value of 13±3 nmol l−1, making it 16 and three times more potent than cariporide IC50: 209±75 nmol l−1, P<0.01) and eniporide (IC50: 40±11 nmol l−1, P=0.066), respectively. T‐162559 also inhibited rat NHE‐1 with an IC50 value of 14±2 nmol l−1, which was five and three times lower than that of cariporide (IC50: 75±7 nmol l−1, P<0.01) and eniporide (IC50: 44±2 nmol l−1, P<0.01), respectively.
T‐162559 inhibited, in a concentration‐dependent manner, the reduction in cardiac contractility, progression of cardiac contracture, and increase in lactate dehydrogenase release after global ischaemia and reperfusion in perfused rat hearts. The inhibitory effects of T‐162559 were observed at a lower concentration range (10 – 100 nmol l−1) than with cariporide and eniporide. T‐162559 did not alter basal cardiac contractility or coronary flow after reperfusion, suggesting that it exerts direct cardioprotective effects on the heart.
Intravenous administration of T‐162559 (0.03 and 0.1 mg kg−1) significantly inhibited the progression of myocardial infarction induced by left coronary artery occlusion and reperfusion in rabbits; the infarct size normalized by area at risk was 74±6% in the vehicle group, and 47±5% and 51±7% in the T‐162559‐0.03 mg kg−1 and T‐162559‐0.1 mg kg−1 groups (both P<0.05), respectively.
These results indicate that the new structural NHE‐1 inhibitor T‐162559 is more potent than cariporide and eniporide and possesses a cardioprotective effect against ischaemia and reperfusion injury in rat and rabbit models.
British Journal of Pharmacology (2002) 135, 1995–2003; doi:10.1038/sj.bjp.0704647</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Platelets - drug effects</subject><subject>Blood Platelets - metabolism</subject><subject>cardioprotection</subject><subject>Cardiotonic Agents - administration & dosage</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cardiovascular system</subject><subject>cariporide</subject><subject>Dose-Response Relationship, Drug</subject><subject>eniporide</subject><subject>Guanidines - administration & dosage</subject><subject>Guanidines - chemistry</subject><subject>Guanidines - pharmacology</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Injections, Intravenous</subject><subject>ischaemia‐reperfusion</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>myocardial infarction</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - prevention & control</subject><subject>Myocardial Ischemia - drug therapy</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Na+‐H+ exchanger</subject><subject>Pharmacology. Drug treatments</subject><subject>Quinolines - administration & dosage</subject><subject>Quinolines - chemistry</subject><subject>Quinolines - pharmacology</subject><subject>Rabbits</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sodium-Hydrogen Exchangers - antagonists & inhibitors</subject><subject>Sulfones - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc1u1DAUhS0EokNhyxJZSHRTMvjGv9kg0QqYShWwKGvLcZwZR5l4sJOB2fEIPCNPgquJKLBhYVnW-e65xzoIPQWyBELVq9Qt6263JJIwweQ9tAAmRcGpgvtoQQiRBYBSJ-hRSh0hWZT8IToBqHilCF0gczXgvR9jwGZosL997APebUzcGhv6sD7g0GKD0xgnO07R9P0BD2HvevzBnP_8_mN1jt03uzHD2uXxja_9GOJLfJMlECXn1WP0oDV9ck_m-xR9fvf25nJVXH98f3X55rqwTElVAFUVI4pBzYQwUEkliKzrBphpFa95LevSMmlZ2crGEcJI41rCG8oMk20p6Cl6ffTdTfXWNdYNY06rd9FvTTzoYLz-Wxn8Rq_DXgOXlEKZDc5mgxi-TC6NeuuTdX1vBhempCUIIiTnGXz-D9iFKQ75c7oECVU-MkPLI2RjSCm69ncSIPq2Op06navTc3V54Nmf-e_wuasMvJgBk6zp22gG69MdR4VikpHM0SP31ffu8J-1-uLTioFQ9BffLbMV</recordid><startdate>200204</startdate><enddate>200204</enddate><creator>Kusumoto, Keiji</creator><creator>Igata, Hideki</creator><creator>Abe, Akemi</creator><creator>Ikeda, Shota</creator><creator>Tsuboi, Ayako</creator><creator>Imamiya, Eikoh</creator><creator>Fukumoto, Shoji</creator><creator>Shiraishi, Mitsuru</creator><creator>Watanabe, Toshifumi</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</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>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>7X8</scope><scope>5PM</scope></search><sort><creationdate>200204</creationdate><title>In vitro and in vivo pharmacology of a structurally novel Na+‐H+ exchange inhibitor, T‐162559</title><author>Kusumoto, Keiji ; Igata, Hideki ; Abe, Akemi ; Ikeda, Shota ; Tsuboi, Ayako ; Imamiya, Eikoh ; Fukumoto, Shoji ; Shiraishi, Mitsuru ; Watanabe, Toshifumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4878-138940841b466a1978607bbd14af85b5b7b2c47c42f7de0040def05d34a47f263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Platelets - drug effects</topic><topic>Blood Platelets - metabolism</topic><topic>cardioprotection</topic><topic>Cardiotonic Agents - administration & dosage</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cardiovascular system</topic><topic>cariporide</topic><topic>Dose-Response Relationship, Drug</topic><topic>eniporide</topic><topic>Guanidines - administration & dosage</topic><topic>Guanidines - chemistry</topic><topic>Guanidines - pharmacology</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Injections, Intravenous</topic><topic>ischaemia‐reperfusion</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>myocardial infarction</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - prevention & control</topic><topic>Myocardial Ischemia - drug therapy</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Na+‐H+ exchanger</topic><topic>Pharmacology. Drug treatments</topic><topic>Quinolines - administration & dosage</topic><topic>Quinolines - chemistry</topic><topic>Quinolines - pharmacology</topic><topic>Rabbits</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sodium-Hydrogen Exchangers - antagonists & inhibitors</topic><topic>Sulfones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kusumoto, Keiji</creatorcontrib><creatorcontrib>Igata, Hideki</creatorcontrib><creatorcontrib>Abe, Akemi</creatorcontrib><creatorcontrib>Ikeda, Shota</creatorcontrib><creatorcontrib>Tsuboi, Ayako</creatorcontrib><creatorcontrib>Imamiya, Eikoh</creatorcontrib><creatorcontrib>Fukumoto, Shoji</creatorcontrib><creatorcontrib>Shiraishi, Mitsuru</creatorcontrib><creatorcontrib>Watanabe, Toshifumi</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>Proquest Central</collection><collection>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>Biological Science Database</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>MEDLINE - Academic</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>Kusumoto, Keiji</au><au>Igata, Hideki</au><au>Abe, Akemi</au><au>Ikeda, Shota</au><au>Tsuboi, Ayako</au><au>Imamiya, Eikoh</au><au>Fukumoto, Shoji</au><au>Shiraishi, Mitsuru</au><au>Watanabe, Toshifumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In vitro and in vivo pharmacology of a structurally novel Na+‐H+ exchange inhibitor, T‐162559</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2002-04</date><risdate>2002</risdate><volume>135</volume><issue>8</issue><spage>1995</spage><epage>2003</epage><pages>1995-2003</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>We investigated the inhibitory effects of a non‐acylguanidine Na+‐H+ exchange (NHE) inhibitor, T‐162559 ((5E,7S)‐[7‐(5‐fluoro‐2‐methylphenyl)‐4‐methyl‐7,8‐dihydro‐5(6H)‐quinolinylideneamino] guanidine dimethanesulphonate), on NHE‐1, and its cardioprotective effect against ischaemia and reperfusion injury in rats and rabbits.
T‐162559 inhibited human platelet NHE‐1 in a concentration‐dependent manner, with an IC50 value of 13±3 nmol l−1, making it 16 and three times more potent than cariporide IC50: 209±75 nmol l−1, P<0.01) and eniporide (IC50: 40±11 nmol l−1, P=0.066), respectively. T‐162559 also inhibited rat NHE‐1 with an IC50 value of 14±2 nmol l−1, which was five and three times lower than that of cariporide (IC50: 75±7 nmol l−1, P<0.01) and eniporide (IC50: 44±2 nmol l−1, P<0.01), respectively.
T‐162559 inhibited, in a concentration‐dependent manner, the reduction in cardiac contractility, progression of cardiac contracture, and increase in lactate dehydrogenase release after global ischaemia and reperfusion in perfused rat hearts. The inhibitory effects of T‐162559 were observed at a lower concentration range (10 – 100 nmol l−1) than with cariporide and eniporide. T‐162559 did not alter basal cardiac contractility or coronary flow after reperfusion, suggesting that it exerts direct cardioprotective effects on the heart.
Intravenous administration of T‐162559 (0.03 and 0.1 mg kg−1) significantly inhibited the progression of myocardial infarction induced by left coronary artery occlusion and reperfusion in rabbits; the infarct size normalized by area at risk was 74±6% in the vehicle group, and 47±5% and 51±7% in the T‐162559‐0.03 mg kg−1 and T‐162559‐0.1 mg kg−1 groups (both P<0.05), respectively.
These results indicate that the new structural NHE‐1 inhibitor T‐162559 is more potent than cariporide and eniporide and possesses a cardioprotective effect against ischaemia and reperfusion injury in rat and rabbit models.
British Journal of Pharmacology (2002) 135, 1995–2003; doi:10.1038/sj.bjp.0704647</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>11959803</pmid><doi>10.1038/sj.bjp.0704647</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0007-1188 |
| ispartof | British journal of pharmacology, 2002-04, Vol.135 (8), p.1995-2003 |
| issn | 0007-1188 1476-5381 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1573312 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via Wiley Online Library; Wiley Online Library (Open Access Collection); PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Blood Platelets - drug effects Blood Platelets - metabolism cardioprotection Cardiotonic Agents - administration & dosage Cardiotonic Agents - pharmacology Cardiovascular system cariporide Dose-Response Relationship, Drug eniporide Guanidines - administration & dosage Guanidines - chemistry Guanidines - pharmacology Humans In Vitro Techniques Injections, Intravenous ischaemia‐reperfusion Male Medical sciences Miscellaneous myocardial infarction Myocardial Infarction - pathology Myocardial Infarction - prevention & control Myocardial Ischemia - drug therapy Myocardial Reperfusion Injury - drug therapy Na+‐H+ exchanger Pharmacology. Drug treatments Quinolines - administration & dosage Quinolines - chemistry Quinolines - pharmacology Rabbits Rats Rats, Wistar Sodium-Hydrogen Exchangers - antagonists & inhibitors Sulfones - pharmacology |
| title | In vitro and in vivo pharmacology of a structurally novel Na+‐H+ exchange inhibitor, T‐162559 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-14T10%3A30%3A23IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=In%20vitro%20and%20in%20vivo%20pharmacology%20of%20a%20structurally%20novel%20Na+%E2%80%90H+%20exchange%20inhibitor,%20T%E2%80%90162559&rft.jtitle=British%20journal%20of%20pharmacology&rft.au=Kusumoto,%20Keiji&rft.date=2002-04&rft.volume=135&rft.issue=8&rft.spage=1995&rft.epage=2003&rft.pages=1995-2003&rft.issn=0007-1188&rft.eissn=1476-5381&rft.coden=BJPCBM&rft_id=info:doi/10.1038/sj.bjp.0704647&rft_dat=%3Cproquest_pubme%3E71606755%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=217191717&rft_id=info:pmid/11959803&rfr_iscdi=true |