Determinants of natriuretic peptide gene expression
The cardiac natriuretic peptides (NP) atrial natriuretic factor or peptide (ANF or ANP) and brain natriuretic peptide (BNP) are polypeptide hormones synthesized, stored and secreted mainly by cardiac muscle cells (cardiocytes) of the atria of the heart. Both ANF and BNP are co-stored in storage gran...
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Veröffentlicht in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2005-06, Vol.26 (6), p.933-943 |
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description | The cardiac natriuretic peptides (NP) atrial natriuretic factor or peptide (ANF or ANP) and brain natriuretic peptide (BNP) are polypeptide hormones synthesized, stored and secreted mainly by cardiac muscle cells (cardiocytes) of the atria of the heart. Both ANF and BNP are co-stored in storage granules referred to as specific atrial granules. The biological properties of NP include modulation of intrinsic renal mechanisms, the sympathetic nervous system, the rennin–angiotensin–aldosterone system (RAAS) and other determinants, of fluid volume, vascular tone and renal function.
Studies on the control of baseline and stimulated ANF synthesis and secretion indicate at least two types of regulated secretory processes in atrial cardiocytes: one is stretch-stimulated and pertussis toxin (PTX) sensitive and the other is Gq-mediated and is PTX insensitive. Baseline ANF secretion is also PTX insensitive. In vivo, it is conceivable that the first process mediates stimulated ANF secretion brought about by changes in central venous return and subsequent atrial muscle stretch as observed in acute extracellular fluid volume expansion. The second type of stimulation is brought about by sustained hemodynamic and neuroendocrine stimuli such as those observed in congestive heart failure. |
doi_str_mv | 10.1016/j.peptides.2004.12.022 |
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Studies on the control of baseline and stimulated ANF synthesis and secretion indicate at least two types of regulated secretory processes in atrial cardiocytes: one is stretch-stimulated and pertussis toxin (PTX) sensitive and the other is Gq-mediated and is PTX insensitive. Baseline ANF secretion is also PTX insensitive. In vivo, it is conceivable that the first process mediates stimulated ANF secretion brought about by changes in central venous return and subsequent atrial muscle stretch as observed in acute extracellular fluid volume expansion. The second type of stimulation is brought about by sustained hemodynamic and neuroendocrine stimuli such as those observed in congestive heart failure.</description><identifier>ISSN: 0196-9781</identifier><identifier>EISSN: 1873-5169</identifier><identifier>DOI: 10.1016/j.peptides.2004.12.022</identifier><identifier>PMID: 15911063</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amino Acid Sequence ; ANF ; Animals ; Atrial Natriuretic Factor - biosynthesis ; Atrial Natriuretic Factor - genetics ; BNP ; Calcium - metabolism ; Exons ; Gene Expression Regulation ; Gene Expression Regulation, Developmental ; GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism ; Heart Failure ; Hemodynamics ; Humans ; Introns ; Models, Biological ; Molecular Sequence Data ; Myocytes, Cardiac - metabolism ; Natriuretic peptide ; Pertussis Toxin - pharmacology ; Signal Transduction</subject><ispartof>Peptides (New York, N.Y. : 1980), 2005-06, Vol.26 (6), p.933-943</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-e1531888b3f6fbaea5b0b5d835c0ef375f4c0f543e1851af09b4eb183d438bdc3</citedby><cites>FETCH-LOGICAL-c463t-e1531888b3f6fbaea5b0b5d835c0ef375f4c0f543e1851af09b4eb183d438bdc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.peptides.2004.12.022$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15911063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McGrath, Monica Forero</creatorcontrib><creatorcontrib>de Bold, Adolfo J.</creatorcontrib><title>Determinants of natriuretic peptide gene expression</title><title>Peptides (New York, N.Y. : 1980)</title><addtitle>Peptides</addtitle><description>The cardiac natriuretic peptides (NP) atrial natriuretic factor or peptide (ANF or ANP) and brain natriuretic peptide (BNP) are polypeptide hormones synthesized, stored and secreted mainly by cardiac muscle cells (cardiocytes) of the atria of the heart. Both ANF and BNP are co-stored in storage granules referred to as specific atrial granules. The biological properties of NP include modulation of intrinsic renal mechanisms, the sympathetic nervous system, the rennin–angiotensin–aldosterone system (RAAS) and other determinants, of fluid volume, vascular tone and renal function.
Studies on the control of baseline and stimulated ANF synthesis and secretion indicate at least two types of regulated secretory processes in atrial cardiocytes: one is stretch-stimulated and pertussis toxin (PTX) sensitive and the other is Gq-mediated and is PTX insensitive. Baseline ANF secretion is also PTX insensitive. In vivo, it is conceivable that the first process mediates stimulated ANF secretion brought about by changes in central venous return and subsequent atrial muscle stretch as observed in acute extracellular fluid volume expansion. The second type of stimulation is brought about by sustained hemodynamic and neuroendocrine stimuli such as those observed in congestive heart failure.</description><subject>Amino Acid Sequence</subject><subject>ANF</subject><subject>Animals</subject><subject>Atrial Natriuretic Factor - biosynthesis</subject><subject>Atrial Natriuretic Factor - genetics</subject><subject>BNP</subject><subject>Calcium - metabolism</subject><subject>Exons</subject><subject>Gene Expression Regulation</subject><subject>Gene Expression Regulation, Developmental</subject><subject>GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism</subject><subject>Heart Failure</subject><subject>Hemodynamics</subject><subject>Humans</subject><subject>Introns</subject><subject>Models, Biological</subject><subject>Molecular Sequence Data</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Natriuretic peptide</subject><subject>Pertussis Toxin - pharmacology</subject><subject>Signal Transduction</subject><issn>0196-9781</issn><issn>1873-5169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkDtPwzAURi0EoqXwF6pMbAm-cezYG6g8pUosMFuJc41cNQ9sB8G_J1WLGDvd5Xz3SIeQJdAMKIibTTbgEF2DIcspLTLIM5rnJ2QOsmQpB6FOyZyCEqkqJczIRQgbOoGFkudkBlwBUMHmhN1jRN-6rupiSHqbdFX0bvQYnUkOiuQDO0zwe_AYguu7S3Jmq23Aq8NdkPfHh7fVc7p-fXpZ3a1TUwgWUwTOQEpZMytsXWHFa1rzRjJuKFpWclsYannBECSHylJVF1iDZE3BZN0YtiDX-7-D7z9HDFG3LhjcbqsO-zFoUUrBciWOgqAUz3muJlDsQeP7EDxaPXjXVv5HA9W7rnqj_7rqXVcNuZ66TsPlwTDWLTb_s0PICbjdAzgF-XLodTAOO4ON82iibnp3zPELy1uNIQ</recordid><startdate>20050601</startdate><enddate>20050601</enddate><creator>McGrath, Monica Forero</creator><creator>de Bold, Adolfo J.</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050601</creationdate><title>Determinants of natriuretic peptide gene expression</title><author>McGrath, Monica Forero ; de Bold, Adolfo J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-e1531888b3f6fbaea5b0b5d835c0ef375f4c0f543e1851af09b4eb183d438bdc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Amino Acid Sequence</topic><topic>ANF</topic><topic>Animals</topic><topic>Atrial Natriuretic Factor - biosynthesis</topic><topic>Atrial Natriuretic Factor - genetics</topic><topic>BNP</topic><topic>Calcium - metabolism</topic><topic>Exons</topic><topic>Gene Expression Regulation</topic><topic>Gene Expression Regulation, Developmental</topic><topic>GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism</topic><topic>Heart Failure</topic><topic>Hemodynamics</topic><topic>Humans</topic><topic>Introns</topic><topic>Models, Biological</topic><topic>Molecular Sequence Data</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Natriuretic peptide</topic><topic>Pertussis Toxin - pharmacology</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McGrath, Monica Forero</creatorcontrib><creatorcontrib>de Bold, Adolfo J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Peptides (New York, N.Y. : 1980)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McGrath, Monica Forero</au><au>de Bold, Adolfo J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Determinants of natriuretic peptide gene expression</atitle><jtitle>Peptides (New York, N.Y. : 1980)</jtitle><addtitle>Peptides</addtitle><date>2005-06-01</date><risdate>2005</risdate><volume>26</volume><issue>6</issue><spage>933</spage><epage>943</epage><pages>933-943</pages><issn>0196-9781</issn><eissn>1873-5169</eissn><abstract>The cardiac natriuretic peptides (NP) atrial natriuretic factor or peptide (ANF or ANP) and brain natriuretic peptide (BNP) are polypeptide hormones synthesized, stored and secreted mainly by cardiac muscle cells (cardiocytes) of the atria of the heart. Both ANF and BNP are co-stored in storage granules referred to as specific atrial granules. The biological properties of NP include modulation of intrinsic renal mechanisms, the sympathetic nervous system, the rennin–angiotensin–aldosterone system (RAAS) and other determinants, of fluid volume, vascular tone and renal function.
Studies on the control of baseline and stimulated ANF synthesis and secretion indicate at least two types of regulated secretory processes in atrial cardiocytes: one is stretch-stimulated and pertussis toxin (PTX) sensitive and the other is Gq-mediated and is PTX insensitive. Baseline ANF secretion is also PTX insensitive. In vivo, it is conceivable that the first process mediates stimulated ANF secretion brought about by changes in central venous return and subsequent atrial muscle stretch as observed in acute extracellular fluid volume expansion. The second type of stimulation is brought about by sustained hemodynamic and neuroendocrine stimuli such as those observed in congestive heart failure.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15911063</pmid><doi>10.1016/j.peptides.2004.12.022</doi><tpages>11</tpages></addata></record> |
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subjects | Amino Acid Sequence ANF Animals Atrial Natriuretic Factor - biosynthesis Atrial Natriuretic Factor - genetics BNP Calcium - metabolism Exons Gene Expression Regulation Gene Expression Regulation, Developmental GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism Heart Failure Hemodynamics Humans Introns Models, Biological Molecular Sequence Data Myocytes, Cardiac - metabolism Natriuretic peptide Pertussis Toxin - pharmacology Signal Transduction |
title | Determinants of natriuretic peptide gene expression |
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