Cardiac Neurobiology of Nitric Oxide Synthases
: Nitric oxide (NO) is a potent modulator of cardiac and vascular regulation. Its role in cardiac‐autonomic neural signaling has received much attention over the last decade because of the ability of NO to alter cardiac sympathovagal balance to favor more anti‐arrhythmic states. Complexity and contr...
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Veröffentlicht in: | Annals of the New York Academy of Sciences 2005-06, Vol.1047 (1), p.183-196 |
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description | : Nitric oxide (NO) is a potent modulator of cardiac and vascular regulation. Its role in cardiac‐autonomic neural signaling has received much attention over the last decade because of the ability of NO to alter cardiac sympathovagal balance to favor more anti‐arrhythmic states. Complexity and controversy have arisen, however, because of the numerous sources of NO in the brain, peripheral nerves, and cardiomyocytes, all of which are potential regulators of cardiac excitability and calcium signaling. This review addresses the integrative role of NO as a relatively ubiquitous signaling molecule with respect to cardiac neurobiology. The present idea, that divergent NO‐signaling pathways from multiple sources within the heart and nervous system converge to modulate cardiac excitability and impact on morbidity and mortality in health and disease, is discussed. |
doi_str_mv | 10.1196/annals.1341.017 |
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Its role in cardiac‐autonomic neural signaling has received much attention over the last decade because of the ability of NO to alter cardiac sympathovagal balance to favor more anti‐arrhythmic states. Complexity and controversy have arisen, however, because of the numerous sources of NO in the brain, peripheral nerves, and cardiomyocytes, all of which are potential regulators of cardiac excitability and calcium signaling. This review addresses the integrative role of NO as a relatively ubiquitous signaling molecule with respect to cardiac neurobiology. 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Its role in cardiac‐autonomic neural signaling has received much attention over the last decade because of the ability of NO to alter cardiac sympathovagal balance to favor more anti‐arrhythmic states. Complexity and controversy have arisen, however, because of the numerous sources of NO in the brain, peripheral nerves, and cardiomyocytes, all of which are potential regulators of cardiac excitability and calcium signaling. This review addresses the integrative role of NO as a relatively ubiquitous signaling molecule with respect to cardiac neurobiology. The present idea, that divergent NO‐signaling pathways from multiple sources within the heart and nervous system converge to modulate cardiac excitability and impact on morbidity and mortality in health and disease, is discussed.</description><subject>Animals</subject><subject>autonomic</subject><subject>Autonomic Nervous System - enzymology</subject><subject>Autonomic Nervous System - physiology</subject><subject>Brain</subject><subject>Ca2+ signaling</subject><subject>Calcium Signaling - physiology</subject><subject>Control</subject><subject>Excitation</subject><subject>Exercise</subject><subject>Heart - innervation</subject><subject>Heart - physiology</subject><subject>Heart Rate - physiology</subject><subject>heart regulation</subject><subject>Humans</subject><subject>Models, Cardiovascular</subject><subject>Modulators</subject><subject>Mortality</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Nervous system</subject><subject>Neurobiology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Regulators</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkTtPwzAURi0EgvKY2VAmxJLi62c8ogooUlUEBSG6WI7jgCFtwG4F_fckSgUbnbyc79zr-yF0DLgPoMS5mc9NFftAGfQxyC3UA8lUKgQl26iHsZRppgjdQ_sxvmEMJGNyF-2BwIoyJXqoPzCh8MYmY7cMde7rqn5ZJXWZjP0ieJvcfvvCJZPVfPFqoouHaKdsBrqj9XuAHq8uHwbDdHR7fTO4GKWWSU5TACmI4IV0RcmFI1YSsM7hAiRXTJAil4RzYyzNDDEZEBB5wbmFHBOCS6AH6LTzfoT6c-niQs98tK6qzNzVy6hF8w_MmdoIgqSKM9Yaz_4HhZSq0QLdjHJoj8c5a9DzDrWhjjG4Un8EPzNhpQHrtiHdNaTbhnTTUJM4WcuX-cwVf_y6kgZgHfDlK7fa5NPj54sJZO3SaRfzceG-f2MmvGshqeT6aXyt8XQ4HE3v7rWiPwBaqjw</recordid><startdate>200506</startdate><enddate>200506</enddate><creator>DANSON, EDWARD J.</creator><creator>PATERSON, DAVID J.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7TK</scope><scope>7SP</scope><scope>7SR</scope><scope>7U5</scope><scope>8FD</scope><scope>JG9</scope><scope>L7M</scope><scope>7QP</scope><scope>7X8</scope></search><sort><creationdate>200506</creationdate><title>Cardiac Neurobiology of Nitric Oxide Synthases</title><author>DANSON, EDWARD J. ; PATERSON, DAVID J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4753-1176265d7edf56e2c721cee0d1759462db7255aac38a2a81216bd55c1b0220f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>autonomic</topic><topic>Autonomic Nervous System - enzymology</topic><topic>Autonomic Nervous System - physiology</topic><topic>Brain</topic><topic>Ca2+ signaling</topic><topic>Calcium Signaling - physiology</topic><topic>Control</topic><topic>Excitation</topic><topic>Exercise</topic><topic>Heart - innervation</topic><topic>Heart - physiology</topic><topic>Heart Rate - physiology</topic><topic>heart regulation</topic><topic>Humans</topic><topic>Models, Cardiovascular</topic><topic>Modulators</topic><topic>Mortality</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - metabolism</topic><topic>Nervous system</topic><topic>Neurobiology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Regulators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DANSON, EDWARD J.</creatorcontrib><creatorcontrib>PATERSON, DAVID J.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Electronics & Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Materials Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DANSON, EDWARD J.</au><au>PATERSON, DAVID J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac Neurobiology of Nitric Oxide Synthases</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>2005-06</date><risdate>2005</risdate><volume>1047</volume><issue>1</issue><spage>183</spage><epage>196</epage><pages>183-196</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><abstract>: Nitric oxide (NO) is a potent modulator of cardiac and vascular regulation. 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subjects | Animals autonomic Autonomic Nervous System - enzymology Autonomic Nervous System - physiology Brain Ca2+ signaling Calcium Signaling - physiology Control Excitation Exercise Heart - innervation Heart - physiology Heart Rate - physiology heart regulation Humans Models, Cardiovascular Modulators Mortality Myocardium - enzymology Myocardium - metabolism Nervous system Neurobiology Nitric oxide Nitric Oxide Synthase - metabolism Regulators |
title | Cardiac Neurobiology of Nitric Oxide Synthases |
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