Role of Nitric Oxide in Cardiac β-Adrenoceptor–Inotropic Response
We examined some of the signalling events in the negative modulation of isoproterenol-induced stimulation of contractility in rat isolated atria. Isoproterenol-mediated positive inotropic response is accompanied by the stimulation of nitric oxide synthase (NOS) and an increase in the production of c...
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| Veröffentlicht in: | Cellular signalling 1998-04, Vol.10 (4), p.253-257 |
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| container_title | Cellular signalling |
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| creator | Sterin-Borda, Leonor Genaro, Ana Leiros, Claudia Perez Cremaschi, Graciela Echagüe, Agustina Vila Borda, Enri |
| description | We examined some of the signalling events in the negative modulation of isoproterenol-induced stimulation of contractility in rat isolated atria. Isoproterenol-mediated positive inotropic response is accompanied by the stimulation of nitric oxide synthase (NOS) and an increase in the production of cyclic GMP (cGMP). Inhibition of NOS and guanylate cyclase increased the dose-response curve of isoproterenol on contractility. Inhibitors of calcium flux or calcium calmodulin, but not of protein kinase C, abrogated these mechanisms. The existence of a modulatory negative inotropic–cyclic GMP–mediated mechanism limiting the effect of β-adrenergic stimulation in myocardium is discussed. |
| doi_str_mv | 10.1016/S0898-6568(97)00125-3 |
| format | Article |
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Isoproterenol-mediated positive inotropic response is accompanied by the stimulation of nitric oxide synthase (NOS) and an increase in the production of cyclic GMP (cGMP). Inhibition of NOS and guanylate cyclase increased the dose-response curve of isoproterenol on contractility. Inhibitors of calcium flux or calcium calmodulin, but not of protein kinase C, abrogated these mechanisms. The existence of a modulatory negative inotropic–cyclic GMP–mediated mechanism limiting the effect of β-adrenergic stimulation in myocardium is discussed.</description><identifier>ISSN: 0898-6568</identifier><identifier>EISSN: 1873-3913</identifier><identifier>DOI: 10.1016/S0898-6568(97)00125-3</identifier><identifier>PMID: 9617482</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Animals ; Atrial Function ; Cardiac contractility ; Cardiotonic Agents - pharmacology ; Cyclic GMP - biosynthesis ; Guanylate cyclase ; Heart Atria - enzymology ; Isoproterenol - pharmacology ; Myocardial Contraction - drug effects ; Myocardium - enzymology ; Myocardium - metabolism ; Nitric oxide ; Nitric Oxide - physiology ; Nitric Oxide Synthase - metabolism ; Protein kinase ; Protein Kinase C - metabolism ; Rat atria ; Rats ; Receptors, Adrenergic, beta - drug effects ; Receptors, Adrenergic, beta - physiology ; Stimulation, Chemical ; β-Adrenoceptor</subject><ispartof>Cellular signalling, 1998-04, Vol.10 (4), p.253-257</ispartof><rights>1998 Elsevier Science Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c360t-7a170fc2a1fec90f383dac5971f08a963244f393a57cefdf8d4b6d32c3ed78dc3</citedby><cites>FETCH-LOGICAL-c360t-7a170fc2a1fec90f383dac5971f08a963244f393a57cefdf8d4b6d32c3ed78dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0898656897001253$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9617482$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sterin-Borda, Leonor</creatorcontrib><creatorcontrib>Genaro, Ana</creatorcontrib><creatorcontrib>Leiros, Claudia Perez</creatorcontrib><creatorcontrib>Cremaschi, Graciela</creatorcontrib><creatorcontrib>Echagüe, Agustina Vila</creatorcontrib><creatorcontrib>Borda, Enri</creatorcontrib><title>Role of Nitric Oxide in Cardiac β-Adrenoceptor–Inotropic Response</title><title>Cellular signalling</title><addtitle>Cell Signal</addtitle><description>We examined some of the signalling events in the negative modulation of isoproterenol-induced stimulation of contractility in rat isolated atria. Isoproterenol-mediated positive inotropic response is accompanied by the stimulation of nitric oxide synthase (NOS) and an increase in the production of cyclic GMP (cGMP). Inhibition of NOS and guanylate cyclase increased the dose-response curve of isoproterenol on contractility. Inhibitors of calcium flux or calcium calmodulin, but not of protein kinase C, abrogated these mechanisms. The existence of a modulatory negative inotropic–cyclic GMP–mediated mechanism limiting the effect of β-adrenergic stimulation in myocardium is discussed.</description><subject>Animals</subject><subject>Atrial Function</subject><subject>Cardiac contractility</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cyclic GMP - biosynthesis</subject><subject>Guanylate cyclase</subject><subject>Heart Atria - enzymology</subject><subject>Isoproterenol - pharmacology</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Protein kinase</subject><subject>Protein Kinase C - metabolism</subject><subject>Rat atria</subject><subject>Rats</subject><subject>Receptors, Adrenergic, beta - drug effects</subject><subject>Receptors, Adrenergic, beta - physiology</subject><subject>Stimulation, Chemical</subject><subject>β-Adrenoceptor</subject><issn>0898-6568</issn><issn>1873-3913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtOwzAQhi0EKqVwhEpZIVgE7DiJ7RWqyqtSRaUCa8u1x5JRGwc7RbDjDtyEg3AITkL6ULesZvF__4zmQ6hP8AXBpLx8xFzwtCxKfibYOcYkK1K6h7qEM5pSQeg-6u6QQ3QU40sLFbjMOqgjSsJynnXR9dTPIfE2eXBNcDqZvDsDiauSoQrGKZ38fKcDE6DyGurGh9_Pr1Hlm-DrFp5CrH0V4RgdWDWPcLKdPfR8e_M0vE_Hk7vRcDBONS1xkzJFGLY6U8SCFthSTo3ShWDEYq5ESbM8t1RQVTAN1lhu8llpaKYpGMaNpj10utlbB_-6hNjIhYsa5nNVgV9GyYTIipyyFiw2oA4-xgBW1sEtVPiQBMuVPbm2J1dqpGBybU_SttffHljOFmB2ra2uNr_a5NB--eYgyKgdVBqMC6Ababz758If37SA0g</recordid><startdate>19980401</startdate><enddate>19980401</enddate><creator>Sterin-Borda, Leonor</creator><creator>Genaro, Ana</creator><creator>Leiros, Claudia Perez</creator><creator>Cremaschi, Graciela</creator><creator>Echagüe, Agustina Vila</creator><creator>Borda, Enri</creator><general>Elsevier Inc</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>19980401</creationdate><title>Role of Nitric Oxide in Cardiac β-Adrenoceptor–Inotropic Response</title><author>Sterin-Borda, Leonor ; Genaro, Ana ; Leiros, Claudia Perez ; Cremaschi, Graciela ; Echagüe, Agustina Vila ; Borda, Enri</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c360t-7a170fc2a1fec90f383dac5971f08a963244f393a57cefdf8d4b6d32c3ed78dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Atrial Function</topic><topic>Cardiac contractility</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cyclic GMP - biosynthesis</topic><topic>Guanylate cyclase</topic><topic>Heart Atria - enzymology</topic><topic>Isoproterenol - pharmacology</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - metabolism</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Protein kinase</topic><topic>Protein Kinase C - metabolism</topic><topic>Rat atria</topic><topic>Rats</topic><topic>Receptors, Adrenergic, beta - drug effects</topic><topic>Receptors, Adrenergic, beta - physiology</topic><topic>Stimulation, Chemical</topic><topic>β-Adrenoceptor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sterin-Borda, Leonor</creatorcontrib><creatorcontrib>Genaro, Ana</creatorcontrib><creatorcontrib>Leiros, Claudia Perez</creatorcontrib><creatorcontrib>Cremaschi, Graciela</creatorcontrib><creatorcontrib>Echagüe, Agustina Vila</creatorcontrib><creatorcontrib>Borda, Enri</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>Cellular signalling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sterin-Borda, Leonor</au><au>Genaro, Ana</au><au>Leiros, Claudia Perez</au><au>Cremaschi, Graciela</au><au>Echagüe, Agustina Vila</au><au>Borda, Enri</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Nitric Oxide in Cardiac β-Adrenoceptor–Inotropic Response</atitle><jtitle>Cellular signalling</jtitle><addtitle>Cell Signal</addtitle><date>1998-04-01</date><risdate>1998</risdate><volume>10</volume><issue>4</issue><spage>253</spage><epage>257</epage><pages>253-257</pages><issn>0898-6568</issn><eissn>1873-3913</eissn><abstract>We examined some of the signalling events in the negative modulation of isoproterenol-induced stimulation of contractility in rat isolated atria. Isoproterenol-mediated positive inotropic response is accompanied by the stimulation of nitric oxide synthase (NOS) and an increase in the production of cyclic GMP (cGMP). Inhibition of NOS and guanylate cyclase increased the dose-response curve of isoproterenol on contractility. Inhibitors of calcium flux or calcium calmodulin, but not of protein kinase C, abrogated these mechanisms. The existence of a modulatory negative inotropic–cyclic GMP–mediated mechanism limiting the effect of β-adrenergic stimulation in myocardium is discussed.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>9617482</pmid><doi>10.1016/S0898-6568(97)00125-3</doi><tpages>5</tpages></addata></record> |
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| ispartof | Cellular signalling, 1998-04, Vol.10 (4), p.253-257 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Atrial Function Cardiac contractility Cardiotonic Agents - pharmacology Cyclic GMP - biosynthesis Guanylate cyclase Heart Atria - enzymology Isoproterenol - pharmacology Myocardial Contraction - drug effects Myocardium - enzymology Myocardium - metabolism Nitric oxide Nitric Oxide - physiology Nitric Oxide Synthase - metabolism Protein kinase Protein Kinase C - metabolism Rat atria Rats Receptors, Adrenergic, beta - drug effects Receptors, Adrenergic, beta - physiology Stimulation, Chemical β-Adrenoceptor |
| title | Role of Nitric Oxide in Cardiac β-Adrenoceptor–Inotropic Response |
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