Ventricular expression of natriuretic peptides in Npr1-/- mice with cardiac hypertrophy and fibrosis
1 Department of Medicine, Christchurch School of Medicine, Christchurch, New Zealand; and 2 Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, North Carolina 27599-7525 Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are cardiac hormone...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2002-08, Vol.283 (2), p.H707-H714 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 283 |
| creator | Ellmers, L. J Knowles, J. W Kim, H.-S Smithies, O Maeda, N Cameron, V. A |
| description | 1 Department of Medicine, Christchurch School of
Medicine, Christchurch, New Zealand; and
2 Department of Pathology and Laboratory Medicine,
University of North Carolina, Chapel Hill, North Carolina
27599-7525
Atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) are cardiac hormones that regulate
blood pressure and volume, and exert their biological actions via the
natriuretic peptide receptor-A gene ( Npr1 ). Mice lacking
Npr1 ( Npr / ) have marked cardiac
hypertrophy and fibrosis disproportionate to their increased blood
pressure. This study examined the relationships between ANP and BNP
gene expression, immunoreactivity and fibrosis in cardiac tissue,
circulating ANP levels, and ANP and BNP mRNA during embryogenesis in
Npr1 / mice. Disruption of the
Npr1 signaling pathway resulted in augmented ANP and BNP
gene and ANP protein expression in the cardiac ventricles, most
pronounced for ANP mRNA in females [414 ± 57 in
Npr1 / ng/mg and 124 ± 25 ng/mg in
wild-type (WT) by Taqman assay, P |
| doi_str_mv | 10.1152/ajpheart.00677.2001 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4321891</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71921935</sourcerecordid><originalsourceid>FETCH-LOGICAL-c446t-d7ce1c1675404576e2d18d8d731f060a601a9fe492c6877b4010cb666b6601633</originalsourceid><addsrcrecordid>eNp1UU1v1DAQtSpQuxR-ARLyiVu2HjuxEw5IqKIUqYJL26vltScbV9nE2Ant_nu87LKFAwdrDu_Db-YR8hbYEqDiF-YhdGjitGRMKrXkjMEJWWSEF1CJ5gVZMCFFIUFUZ-RVSg-MsUpJcUrOgAMvOTQL4u5xmKK3c28ixacQMSU_DnRs6WAyMEecvKUBw-QdJuoH-i1EKC4KuvEW6aOfOmpNdN5Y2m0DximOodtSMzja-lUck0-vycvW9AnfHOY5ubv6fHt5Xdx8__L18tNNYctSToVTFsGCVFXJypwUuYPa1U4JaJlkRjIwTYtlw62slVqVDJhdSSnzYyCFOCcf975hXm3Q2d1qptch-o2JWz0ar_9FBt_p9fhTl4JD3UA2eH8wiOOPGdOkNz5Z7Hsz4DgnraDJVxNVJoo90eYFU8T2-AkwvWtH_2lH_25H79rJqnd_53vWHOrIhA97QufX3aOPqPMpcx_9uN7qq7nvb_FpOlrzWmiurxVTOrg2i5f_Fx_jPIvEL_T9tPg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71921935</pqid></control><display><type>article</type><title>Ventricular expression of natriuretic peptides in Npr1-/- mice with cardiac hypertrophy and fibrosis</title><source>MEDLINE</source><source>American Physiological Society</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Ellmers, L. J ; Knowles, J. W ; Kim, H.-S ; Smithies, O ; Maeda, N ; Cameron, V. A</creator><creatorcontrib>Ellmers, L. J ; Knowles, J. W ; Kim, H.-S ; Smithies, O ; Maeda, N ; Cameron, V. A</creatorcontrib><description>1 Department of Medicine, Christchurch School of
Medicine, Christchurch, New Zealand; and
2 Department of Pathology and Laboratory Medicine,
University of North Carolina, Chapel Hill, North Carolina
27599-7525
Atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) are cardiac hormones that regulate
blood pressure and volume, and exert their biological actions via the
natriuretic peptide receptor-A gene ( Npr1 ). Mice lacking
Npr1 ( Npr / ) have marked cardiac
hypertrophy and fibrosis disproportionate to their increased blood
pressure. This study examined the relationships between ANP and BNP
gene expression, immunoreactivity and fibrosis in cardiac tissue,
circulating ANP levels, and ANP and BNP mRNA during embryogenesis in
Npr1 / mice. Disruption of the
Npr1 signaling pathway resulted in augmented ANP and BNP
gene and ANP protein expression in the cardiac ventricles, most
pronounced for ANP mRNA in females [414 ± 57 in
Npr1 / ng/mg and 124 ± 25 ng/mg in
wild-type (WT) by Taqman assay, P < 0.001]. This
increased expression was highly correlated to the degree of cardiac
hypertrophy and was localized to the left ventricle (LV) inner free
wall and to areas of ventricular fibrosis. In contrast, plasma ANP was
significantly greater than WT in male but not female
Npr1 / mice. Increased ANP and BNP gene
expression was observed in Npr1 / embryos
from 16 days of gestation. Our study suggests that cardiac ventricular
expression of ANP and BNP is more closely associated with local
hypertrophy and fibrosis than either systemic blood pressure or
circulating ANP levels.
atrial natriuretic peptide; brain natriuretic peptide</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00677.2001</identifier><identifier>PMID: 12124219</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Atrial Natriuretic Factor - blood ; Atrial Natriuretic Factor - genetics ; Atrial Natriuretic Factor - metabolism ; Cardiomegaly - etiology ; Cardiomegaly - metabolism ; Cardiomyopathies - etiology ; Cardiomyopathies - metabolism ; Cardiomyopathies - pathology ; Embryo, Mammalian - metabolism ; Female ; Fibrosis ; Guanylate Cyclase - deficiency ; Guanylate Cyclase - genetics ; Heart Ventricles ; Hypertension - etiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout - genetics ; Myocardium - metabolism ; Natriuretic Peptide, Brain - blood ; Natriuretic Peptide, Brain - genetics ; Natriuretic Peptide, Brain - metabolism ; Receptors, Atrial Natriuretic Factor - deficiency ; Receptors, Atrial Natriuretic Factor - genetics ; Reference Values ; RNA, Messenger - metabolism</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2002-08, Vol.283 (2), p.H707-H714</ispartof><rights>2002 the American Physiological Society 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-d7ce1c1675404576e2d18d8d731f060a601a9fe492c6877b4010cb666b6601633</citedby><cites>FETCH-LOGICAL-c446t-d7ce1c1675404576e2d18d8d731f060a601a9fe492c6877b4010cb666b6601633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12124219$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ellmers, L. J</creatorcontrib><creatorcontrib>Knowles, J. W</creatorcontrib><creatorcontrib>Kim, H.-S</creatorcontrib><creatorcontrib>Smithies, O</creatorcontrib><creatorcontrib>Maeda, N</creatorcontrib><creatorcontrib>Cameron, V. A</creatorcontrib><title>Ventricular expression of natriuretic peptides in Npr1-/- mice with cardiac hypertrophy and fibrosis</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>1 Department of Medicine, Christchurch School of
Medicine, Christchurch, New Zealand; and
2 Department of Pathology and Laboratory Medicine,
University of North Carolina, Chapel Hill, North Carolina
27599-7525
Atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) are cardiac hormones that regulate
blood pressure and volume, and exert their biological actions via the
natriuretic peptide receptor-A gene ( Npr1 ). Mice lacking
Npr1 ( Npr / ) have marked cardiac
hypertrophy and fibrosis disproportionate to their increased blood
pressure. This study examined the relationships between ANP and BNP
gene expression, immunoreactivity and fibrosis in cardiac tissue,
circulating ANP levels, and ANP and BNP mRNA during embryogenesis in
Npr1 / mice. Disruption of the
Npr1 signaling pathway resulted in augmented ANP and BNP
gene and ANP protein expression in the cardiac ventricles, most
pronounced for ANP mRNA in females [414 ± 57 in
Npr1 / ng/mg and 124 ± 25 ng/mg in
wild-type (WT) by Taqman assay, P < 0.001]. This
increased expression was highly correlated to the degree of cardiac
hypertrophy and was localized to the left ventricle (LV) inner free
wall and to areas of ventricular fibrosis. In contrast, plasma ANP was
significantly greater than WT in male but not female
Npr1 / mice. Increased ANP and BNP gene
expression was observed in Npr1 / embryos
from 16 days of gestation. Our study suggests that cardiac ventricular
expression of ANP and BNP is more closely associated with local
hypertrophy and fibrosis than either systemic blood pressure or
circulating ANP levels.
atrial natriuretic peptide; brain natriuretic peptide</description><subject>Animals</subject><subject>Atrial Natriuretic Factor - blood</subject><subject>Atrial Natriuretic Factor - genetics</subject><subject>Atrial Natriuretic Factor - metabolism</subject><subject>Cardiomegaly - etiology</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomyopathies - etiology</subject><subject>Cardiomyopathies - metabolism</subject><subject>Cardiomyopathies - pathology</subject><subject>Embryo, Mammalian - metabolism</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Guanylate Cyclase - deficiency</subject><subject>Guanylate Cyclase - genetics</subject><subject>Heart Ventricles</subject><subject>Hypertension - etiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout - genetics</subject><subject>Myocardium - metabolism</subject><subject>Natriuretic Peptide, Brain - blood</subject><subject>Natriuretic Peptide, Brain - genetics</subject><subject>Natriuretic Peptide, Brain - metabolism</subject><subject>Receptors, Atrial Natriuretic Factor - deficiency</subject><subject>Receptors, Atrial Natriuretic Factor - genetics</subject><subject>Reference Values</subject><subject>RNA, Messenger - metabolism</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1UU1v1DAQtSpQuxR-ARLyiVu2HjuxEw5IqKIUqYJL26vltScbV9nE2Ant_nu87LKFAwdrDu_Db-YR8hbYEqDiF-YhdGjitGRMKrXkjMEJWWSEF1CJ5gVZMCFFIUFUZ-RVSg-MsUpJcUrOgAMvOTQL4u5xmKK3c28ixacQMSU_DnRs6WAyMEecvKUBw-QdJuoH-i1EKC4KuvEW6aOfOmpNdN5Y2m0DximOodtSMzja-lUck0-vycvW9AnfHOY5ubv6fHt5Xdx8__L18tNNYctSToVTFsGCVFXJypwUuYPa1U4JaJlkRjIwTYtlw62slVqVDJhdSSnzYyCFOCcf975hXm3Q2d1qptch-o2JWz0ar_9FBt_p9fhTl4JD3UA2eH8wiOOPGdOkNz5Z7Hsz4DgnraDJVxNVJoo90eYFU8T2-AkwvWtH_2lH_25H79rJqnd_53vWHOrIhA97QufX3aOPqPMpcx_9uN7qq7nvb_FpOlrzWmiurxVTOrg2i5f_Fx_jPIvEL_T9tPg</recordid><startdate>20020801</startdate><enddate>20020801</enddate><creator>Ellmers, L. J</creator><creator>Knowles, J. W</creator><creator>Kim, H.-S</creator><creator>Smithies, O</creator><creator>Maeda, N</creator><creator>Cameron, V. A</creator><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><scope>5PM</scope></search><sort><creationdate>20020801</creationdate><title>Ventricular expression of natriuretic peptides in Npr1-/- mice with cardiac hypertrophy and fibrosis</title><author>Ellmers, L. J ; Knowles, J. W ; Kim, H.-S ; Smithies, O ; Maeda, N ; Cameron, V. A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-d7ce1c1675404576e2d18d8d731f060a601a9fe492c6877b4010cb666b6601633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Atrial Natriuretic Factor - blood</topic><topic>Atrial Natriuretic Factor - genetics</topic><topic>Atrial Natriuretic Factor - metabolism</topic><topic>Cardiomegaly - etiology</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiomyopathies - etiology</topic><topic>Cardiomyopathies - metabolism</topic><topic>Cardiomyopathies - pathology</topic><topic>Embryo, Mammalian - metabolism</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Guanylate Cyclase - deficiency</topic><topic>Guanylate Cyclase - genetics</topic><topic>Heart Ventricles</topic><topic>Hypertension - etiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout - genetics</topic><topic>Myocardium - metabolism</topic><topic>Natriuretic Peptide, Brain - blood</topic><topic>Natriuretic Peptide, Brain - genetics</topic><topic>Natriuretic Peptide, Brain - metabolism</topic><topic>Receptors, Atrial Natriuretic Factor - deficiency</topic><topic>Receptors, Atrial Natriuretic Factor - genetics</topic><topic>Reference Values</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ellmers, L. J</creatorcontrib><creatorcontrib>Knowles, J. W</creatorcontrib><creatorcontrib>Kim, H.-S</creatorcontrib><creatorcontrib>Smithies, O</creatorcontrib><creatorcontrib>Maeda, N</creatorcontrib><creatorcontrib>Cameron, V. A</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ellmers, L. J</au><au>Knowles, J. W</au><au>Kim, H.-S</au><au>Smithies, O</au><au>Maeda, N</au><au>Cameron, V. A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ventricular expression of natriuretic peptides in Npr1-/- mice with cardiac hypertrophy and fibrosis</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2002-08-01</date><risdate>2002</risdate><volume>283</volume><issue>2</issue><spage>H707</spage><epage>H714</epage><pages>H707-H714</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>1 Department of Medicine, Christchurch School of
Medicine, Christchurch, New Zealand; and
2 Department of Pathology and Laboratory Medicine,
University of North Carolina, Chapel Hill, North Carolina
27599-7525
Atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) are cardiac hormones that regulate
blood pressure and volume, and exert their biological actions via the
natriuretic peptide receptor-A gene ( Npr1 ). Mice lacking
Npr1 ( Npr / ) have marked cardiac
hypertrophy and fibrosis disproportionate to their increased blood
pressure. This study examined the relationships between ANP and BNP
gene expression, immunoreactivity and fibrosis in cardiac tissue,
circulating ANP levels, and ANP and BNP mRNA during embryogenesis in
Npr1 / mice. Disruption of the
Npr1 signaling pathway resulted in augmented ANP and BNP
gene and ANP protein expression in the cardiac ventricles, most
pronounced for ANP mRNA in females [414 ± 57 in
Npr1 / ng/mg and 124 ± 25 ng/mg in
wild-type (WT) by Taqman assay, P < 0.001]. This
increased expression was highly correlated to the degree of cardiac
hypertrophy and was localized to the left ventricle (LV) inner free
wall and to areas of ventricular fibrosis. In contrast, plasma ANP was
significantly greater than WT in male but not female
Npr1 / mice. Increased ANP and BNP gene
expression was observed in Npr1 / embryos
from 16 days of gestation. Our study suggests that cardiac ventricular
expression of ANP and BNP is more closely associated with local
hypertrophy and fibrosis than either systemic blood pressure or
circulating ANP levels.
atrial natriuretic peptide; brain natriuretic peptide</abstract><cop>United States</cop><pmid>12124219</pmid><doi>10.1152/ajpheart.00677.2001</doi></addata></record> |
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| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2002-08, Vol.283 (2), p.H707-H714 |
| issn | 0363-6135 1522-1539 |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4321891 |
| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Atrial Natriuretic Factor - blood Atrial Natriuretic Factor - genetics Atrial Natriuretic Factor - metabolism Cardiomegaly - etiology Cardiomegaly - metabolism Cardiomyopathies - etiology Cardiomyopathies - metabolism Cardiomyopathies - pathology Embryo, Mammalian - metabolism Female Fibrosis Guanylate Cyclase - deficiency Guanylate Cyclase - genetics Heart Ventricles Hypertension - etiology Male Mice Mice, Inbred C57BL Mice, Knockout - genetics Myocardium - metabolism Natriuretic Peptide, Brain - blood Natriuretic Peptide, Brain - genetics Natriuretic Peptide, Brain - metabolism Receptors, Atrial Natriuretic Factor - deficiency Receptors, Atrial Natriuretic Factor - genetics Reference Values RNA, Messenger - metabolism |
| title | Ventricular expression of natriuretic peptides in Npr1-/- mice with cardiac hypertrophy and fibrosis |
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