Evidence for nitric oxide generation in the cardiomyocytes: its augmentation by hypoxia
Recent report suggest that endothelial-dependent relaxant factor, recoggnized as nitric oxide (NO), reduces myocardial contractility. Here, we showed that both exposures to acetylcholine and bradykinin for 30 min increased cyclic guanylate monophosphate (cyclic GMP) in isolated rat cardiomyocytes. T...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 1995-10, Vol.27 (10), p.2149-2154 |
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| container_issue | 10 |
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| container_title | Journal of molecular and cellular cardiology |
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| creator | Kitakaze, Masafumi Node, Koichi Komamura, Kazuo Minamino, Tetsuo Inoue, Michitoshi Hori, Masatsugu Kamada, Takenobu |
| description | Recent report suggest that endothelial-dependent relaxant factor, recoggnized as nitric oxide (NO), reduces myocardial contractility. Here, we showed that both exposures to acetylcholine and bradykinin for 30 min increased cyclic guanylate monophosphate (cyclic GMP) in isolated rat cardiomyocytes. These increases in cyclic GMP were blunted ny NW-nitro-L-arginine methyl ester (L-NAME). an inhibitor of NO synthase. Hypoxia augmented the cyclic GMP accumulation due to exposures to acetylcholine and bradykinin, which were blunted by L-NAME. The increases in cyclic GMP due to acetylcholine and bradykinin during normoxic and hypoxic conditions were not blunted by aminoguanidine, an inhibitor of inducible NO syntase. These findongs revealed cyclase, which was augmented by hypoxia. NO production, through synthase in cardiomyocytes, may constitute autocrine regulations of myocardial contractility and paracrine regulations of coronary vasodilation and platelet aggregation. |
| doi_str_mv | 10.1016/S0022-2828(95)91335-1 |
| format | Article |
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Here, we showed that both exposures to acetylcholine and bradykinin for 30 min increased cyclic guanylate monophosphate (cyclic GMP) in isolated rat cardiomyocytes. These increases in cyclic GMP were blunted ny NW-nitro-L-arginine methyl ester (L-NAME). an inhibitor of NO synthase. Hypoxia augmented the cyclic GMP accumulation due to exposures to acetylcholine and bradykinin, which were blunted by L-NAME. The increases in cyclic GMP due to acetylcholine and bradykinin during normoxic and hypoxic conditions were not blunted by aminoguanidine, an inhibitor of inducible NO syntase. These findongs revealed cyclase, which was augmented by hypoxia. NO production, through synthase in cardiomyocytes, may constitute autocrine regulations of myocardial contractility and paracrine regulations of coronary vasodilation and platelet aggregation.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1016/S0022-2828(95)91335-1</identifier><identifier>PMID: 8576931</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Acetylcholine - pharmacology ; Animals ; Arginine - analogs & derivatives ; Arginine - pharmacology ; Bradykinin - pharmacology ; Cell Hypoxia ; Cyclic AMP - biosynthesis ; Cyclic GMP - biosynthesis ; Guanidines - pharmacology ; Guanylate Cyclase - metabolism ; Heart - drug effects ; Male ; Myocardium - cytology ; Myocardium - metabolism ; NG-Nitroarginine Methyl Ester ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Rats ; Rats, Wistar ; Stimulation, Chemical</subject><ispartof>Journal of molecular and cellular cardiology, 1995-10, Vol.27 (10), p.2149-2154</ispartof><rights>1995 Academic Press Limited</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c360t-7fd7750b7b7d782c86033a46783f7426de7a287fe6b14b7c7553196aae12bfaa3</citedby><cites>FETCH-LOGICAL-c360t-7fd7750b7b7d782c86033a46783f7426de7a287fe6b14b7c7553196aae12bfaa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0022-2828(95)91335-1$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8576931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kitakaze, Masafumi</creatorcontrib><creatorcontrib>Node, Koichi</creatorcontrib><creatorcontrib>Komamura, Kazuo</creatorcontrib><creatorcontrib>Minamino, Tetsuo</creatorcontrib><creatorcontrib>Inoue, Michitoshi</creatorcontrib><creatorcontrib>Hori, Masatsugu</creatorcontrib><creatorcontrib>Kamada, Takenobu</creatorcontrib><title>Evidence for nitric oxide generation in the cardiomyocytes: its augmentation by hypoxia</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>Recent report suggest that endothelial-dependent relaxant factor, recoggnized as nitric oxide (NO), reduces myocardial contractility. Here, we showed that both exposures to acetylcholine and bradykinin for 30 min increased cyclic guanylate monophosphate (cyclic GMP) in isolated rat cardiomyocytes. These increases in cyclic GMP were blunted ny NW-nitro-L-arginine methyl ester (L-NAME). an inhibitor of NO synthase. Hypoxia augmented the cyclic GMP accumulation due to exposures to acetylcholine and bradykinin, which were blunted by L-NAME. The increases in cyclic GMP due to acetylcholine and bradykinin during normoxic and hypoxic conditions were not blunted by aminoguanidine, an inhibitor of inducible NO syntase. These findongs revealed cyclase, which was augmented by hypoxia. NO production, through synthase in cardiomyocytes, may constitute autocrine regulations of myocardial contractility and paracrine regulations of coronary vasodilation and platelet aggregation.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - pharmacology</subject><subject>Bradykinin - pharmacology</subject><subject>Cell Hypoxia</subject><subject>Cyclic AMP - biosynthesis</subject><subject>Cyclic GMP - biosynthesis</subject><subject>Guanidines - pharmacology</subject><subject>Guanylate Cyclase - metabolism</subject><subject>Heart - drug effects</subject><subject>Male</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>NG-Nitroarginine Methyl Ester</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Stimulation, Chemical</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtPwzAQhC0EKqXwEyr5hOAQsOM4drggVJWHVIkDII6W42xaoyYutluRf0_6EFdOK-3M7Gg_hMaU3FBC89s3QtI0SWUqrwp-XVDGeEKP0JCSgieSy-wYDf8sp-gshC9CSJExNkADyUVeMDpEn9ONraA1gGvncWujtwa7n36H59CC19G6FtsWxwVgo31lXdM500UId9jGgPV63kAb976yw4tu1cf1OTqp9TLAxWGO0Mfj9H3ynMxen14mD7PEsJzERNSVEJyUohSVkKmROWFMZ7mQrBZZmlcgdCpFDXlJs1IYwTmjRa410LSstWYjdLm_u_Luew0hqsYGA8ulbsGtgxJCFDTr4YwQ3xuNdyF4qNXK20b7TlGitkDVDqja0lIFVzugiva58aFgXTZQ_aUOBHv9fq9D_-XGglfB2C3QynowUVXO_tPwC5D5hhE</recordid><startdate>19951001</startdate><enddate>19951001</enddate><creator>Kitakaze, Masafumi</creator><creator>Node, Koichi</creator><creator>Komamura, Kazuo</creator><creator>Minamino, Tetsuo</creator><creator>Inoue, Michitoshi</creator><creator>Hori, Masatsugu</creator><creator>Kamada, Takenobu</creator><general>Elsevier Ltd</general><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>19951001</creationdate><title>Evidence for nitric oxide generation in the cardiomyocytes: its augmentation by hypoxia</title><author>Kitakaze, Masafumi ; Node, Koichi ; Komamura, Kazuo ; Minamino, Tetsuo ; Inoue, Michitoshi ; Hori, Masatsugu ; Kamada, Takenobu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c360t-7fd7750b7b7d782c86033a46783f7426de7a287fe6b14b7c7553196aae12bfaa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - pharmacology</topic><topic>Bradykinin - pharmacology</topic><topic>Cell Hypoxia</topic><topic>Cyclic AMP - biosynthesis</topic><topic>Cyclic GMP - biosynthesis</topic><topic>Guanidines - pharmacology</topic><topic>Guanylate Cyclase - metabolism</topic><topic>Heart - drug effects</topic><topic>Male</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>NG-Nitroarginine Methyl Ester</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Stimulation, Chemical</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kitakaze, Masafumi</creatorcontrib><creatorcontrib>Node, Koichi</creatorcontrib><creatorcontrib>Komamura, Kazuo</creatorcontrib><creatorcontrib>Minamino, Tetsuo</creatorcontrib><creatorcontrib>Inoue, Michitoshi</creatorcontrib><creatorcontrib>Hori, Masatsugu</creatorcontrib><creatorcontrib>Kamada, Takenobu</creatorcontrib><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>Kitakaze, Masafumi</au><au>Node, Koichi</au><au>Komamura, Kazuo</au><au>Minamino, Tetsuo</au><au>Inoue, Michitoshi</au><au>Hori, Masatsugu</au><au>Kamada, Takenobu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence for nitric oxide generation in the cardiomyocytes: its augmentation by hypoxia</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>1995-10-01</date><risdate>1995</risdate><volume>27</volume><issue>10</issue><spage>2149</spage><epage>2154</epage><pages>2149-2154</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>Recent report suggest that endothelial-dependent relaxant factor, recoggnized as nitric oxide (NO), reduces myocardial contractility. Here, we showed that both exposures to acetylcholine and bradykinin for 30 min increased cyclic guanylate monophosphate (cyclic GMP) in isolated rat cardiomyocytes. These increases in cyclic GMP were blunted ny NW-nitro-L-arginine methyl ester (L-NAME). an inhibitor of NO synthase. Hypoxia augmented the cyclic GMP accumulation due to exposures to acetylcholine and bradykinin, which were blunted by L-NAME. The increases in cyclic GMP due to acetylcholine and bradykinin during normoxic and hypoxic conditions were not blunted by aminoguanidine, an inhibitor of inducible NO syntase. These findongs revealed cyclase, which was augmented by hypoxia. NO production, through synthase in cardiomyocytes, may constitute autocrine regulations of myocardial contractility and paracrine regulations of coronary vasodilation and platelet aggregation.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>8576931</pmid><doi>10.1016/S0022-2828(95)91335-1</doi><tpages>6</tpages></addata></record> |
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| ispartof | Journal of molecular and cellular cardiology, 1995-10, Vol.27 (10), p.2149-2154 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Acetylcholine - pharmacology Animals Arginine - analogs & derivatives Arginine - pharmacology Bradykinin - pharmacology Cell Hypoxia Cyclic AMP - biosynthesis Cyclic GMP - biosynthesis Guanidines - pharmacology Guanylate Cyclase - metabolism Heart - drug effects Male Myocardium - cytology Myocardium - metabolism NG-Nitroarginine Methyl Ester Nitric Oxide - biosynthesis Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism Rats Rats, Wistar Stimulation, Chemical |
| title | Evidence for nitric oxide generation in the cardiomyocytes: its augmentation by hypoxia |
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