High salt intake damages the heart through activation of cardiac (pro) renin receptors even at an early stage of hypertension
It has not yet been fully elucidated whether cardiac tissue levels of prorenin, renin and (P)RR are activated in hypertension with a high salt intake. We hypothesized that a high salt intake activates the cardiac tissue renin angiotensin system and prorenin-(pro)renin receptor system, and damages th...
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| Veröffentlicht in: | PloS one 2015-03, Vol.10 (3), p.e0120453 |
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| creator | Hayakawa, Yuka Aoyama, Takuma Yokoyama, Chiharu Okamoto, Chihiro Komaki, Hisaaki Minatoguchi, Shingo Iwasa, Masamitsu Yamada, Yoshihisa Kawamura, Itta Kawasaki, Masanori Nishigaki, Kazuhiko Mikami, Atsushi Suzuki, Fumiaki Minatoguchi, Shinya |
| description | It has not yet been fully elucidated whether cardiac tissue levels of prorenin, renin and (P)RR are activated in hypertension with a high salt intake. We hypothesized that a high salt intake activates the cardiac tissue renin angiotensin system and prorenin-(pro)renin receptor system, and damages the heart at an early stage of hypertension.
Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) received regular (normal-salt diet, 0.9%) and high-salt (8.9%) chow for 6 weeks from 6 to 12 weeks of age. The systolic blood pressure, plasma renin activity (PRA) and plasma angiotensin II concentration were measured, and the protein expressions of prorenin, (pro)renin receptor, angiotensinogen, angiotensin II AT1 receptor, ERK1/2, TGF-β, p38MAPK and HSP27 in the myocardium were investigated. The cardiac function was assessed by echocardiography, and histological analysis of the myocardium was performed.
The high-salt diet significantly increased the systolic blood pressure, and significantly reduced the PRA and plasma angiotensin II concentration both in the WKYs and SHRs. Cardiac expressions of prorenin, renin, (P)RR, angiotensinogen, angiotensin II AT1 receptor, phosphorylated (p)-ERK1/2, p-p38MAPK, TGF-β and p-HSP27 were significantly increased by the high salt diet both in the WKYs and SHRs. The high-salt diet significantly increased the interventricular septum thickness and cardiomyocyte size, and accelerated cardiac interstitial and perivascular fibrosis both in the WKYs and SHRs. On the other hand, dilatation of left ventricular end-diastolic dimension and impairment of left ventricular fractional shortening was shown only in salt loaded SHRs.
The high-salt diet markedly accelerated cardiac damage through the stimulation of cardiac (P)RR and angiotensin II AT1 receptor by increasing tissue prorenin, renin and angiotensinogen and the activation of ERK1/2, TGF-β, p38MAPK and HSP27 under higher blood pressure. |
| doi_str_mv | 10.1371/journal.pone.0120453 |
| format | Article |
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Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) received regular (normal-salt diet, 0.9%) and high-salt (8.9%) chow for 6 weeks from 6 to 12 weeks of age. The systolic blood pressure, plasma renin activity (PRA) and plasma angiotensin II concentration were measured, and the protein expressions of prorenin, (pro)renin receptor, angiotensinogen, angiotensin II AT1 receptor, ERK1/2, TGF-β, p38MAPK and HSP27 in the myocardium were investigated. The cardiac function was assessed by echocardiography, and histological analysis of the myocardium was performed.
The high-salt diet significantly increased the systolic blood pressure, and significantly reduced the PRA and plasma angiotensin II concentration both in the WKYs and SHRs. Cardiac expressions of prorenin, renin, (P)RR, angiotensinogen, angiotensin II AT1 receptor, phosphorylated (p)-ERK1/2, p-p38MAPK, TGF-β and p-HSP27 were significantly increased by the high salt diet both in the WKYs and SHRs. The high-salt diet significantly increased the interventricular septum thickness and cardiomyocyte size, and accelerated cardiac interstitial and perivascular fibrosis both in the WKYs and SHRs. On the other hand, dilatation of left ventricular end-diastolic dimension and impairment of left ventricular fractional shortening was shown only in salt loaded SHRs.
The high-salt diet markedly accelerated cardiac damage through the stimulation of cardiac (P)RR and angiotensin II AT1 receptor by increasing tissue prorenin, renin and angiotensinogen and the activation of ERK1/2, TGF-β, p38MAPK and HSP27 under higher blood pressure.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0120453</identifier><identifier>PMID: 25799069</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Angiotensin AT1 receptors ; Angiotensin II ; Angiotensin II - blood ; Angiotensinogen ; Angiotensinogen - genetics ; Angiotensinogen - metabolism ; Angiotensins ; Animals ; Blood ; Blood Pressure ; Body Weight ; Bone morphogenetic proteins ; Cardiology ; Cardiomyocytes ; Damage ; Diet ; Echocardiography ; Fibrosis ; Gene Expression ; Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - metabolism ; Heart ; Heart diseases ; Heart Ventricles - metabolism ; Heart Ventricles - pathology ; Heat shock proteins ; HSP27 Heat-Shock Proteins - genetics ; HSP27 Heat-Shock Proteins - metabolism ; Hsp27 protein ; Hypertension ; Hypertension - etiology ; Hypertension - metabolism ; Hypertension - pathology ; Kidneys ; Kinases ; Laboratory animals ; Lung - pathology ; Male ; Medical research ; Medicine ; Myocardium ; Myocardium - metabolism ; Myocardium - pathology ; Nutrition research ; Organ Size ; p38 Mitogen-Activated Protein Kinases - genetics ; p38 Mitogen-Activated Protein Kinases - metabolism ; Plasma ; Prorenin Receptor ; Rats ; Receptor, Angiotensin, Type 1 - genetics ; Receptor, Angiotensin, Type 1 - metabolism ; Receptors ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; Renin ; Renin - blood ; Renin - genetics ; Rodents ; Salts ; Septum ; Signal Transduction ; Sodium Chloride, Dietary - administration & dosage ; Sodium Chloride, Dietary - adverse effects ; Transforming Growth Factor beta1 - genetics ; Transforming Growth Factor beta1 - metabolism ; Transforming growth factors ; University graduates ; Ventricle</subject><ispartof>PloS one, 2015-03, Vol.10 (3), p.e0120453</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Hayakawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Hayakawa et al 2015 Hayakawa et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-1736a64844d012f864ad4fba339290a82d1613b2eec42d5031628a6ff227c763</citedby><cites>FETCH-LOGICAL-c758t-1736a64844d012f864ad4fba339290a82d1613b2eec42d5031628a6ff227c763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370564/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370564/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25799069$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hayakawa, Yuka</creatorcontrib><creatorcontrib>Aoyama, Takuma</creatorcontrib><creatorcontrib>Yokoyama, Chiharu</creatorcontrib><creatorcontrib>Okamoto, Chihiro</creatorcontrib><creatorcontrib>Komaki, Hisaaki</creatorcontrib><creatorcontrib>Minatoguchi, Shingo</creatorcontrib><creatorcontrib>Iwasa, Masamitsu</creatorcontrib><creatorcontrib>Yamada, Yoshihisa</creatorcontrib><creatorcontrib>Kawamura, Itta</creatorcontrib><creatorcontrib>Kawasaki, Masanori</creatorcontrib><creatorcontrib>Nishigaki, Kazuhiko</creatorcontrib><creatorcontrib>Mikami, Atsushi</creatorcontrib><creatorcontrib>Suzuki, Fumiaki</creatorcontrib><creatorcontrib>Minatoguchi, Shinya</creatorcontrib><title>High salt intake damages the heart through activation of cardiac (pro) renin receptors even at an early stage of hypertension</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>It has not yet been fully elucidated whether cardiac tissue levels of prorenin, renin and (P)RR are activated in hypertension with a high salt intake. We hypothesized that a high salt intake activates the cardiac tissue renin angiotensin system and prorenin-(pro)renin receptor system, and damages the heart at an early stage of hypertension.
Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) received regular (normal-salt diet, 0.9%) and high-salt (8.9%) chow for 6 weeks from 6 to 12 weeks of age. The systolic blood pressure, plasma renin activity (PRA) and plasma angiotensin II concentration were measured, and the protein expressions of prorenin, (pro)renin receptor, angiotensinogen, angiotensin II AT1 receptor, ERK1/2, TGF-β, p38MAPK and HSP27 in the myocardium were investigated. The cardiac function was assessed by echocardiography, and histological analysis of the myocardium was performed.
The high-salt diet significantly increased the systolic blood pressure, and significantly reduced the PRA and plasma angiotensin II concentration both in the WKYs and SHRs. Cardiac expressions of prorenin, renin, (P)RR, angiotensinogen, angiotensin II AT1 receptor, phosphorylated (p)-ERK1/2, p-p38MAPK, TGF-β and p-HSP27 were significantly increased by the high salt diet both in the WKYs and SHRs. The high-salt diet significantly increased the interventricular septum thickness and cardiomyocyte size, and accelerated cardiac interstitial and perivascular fibrosis both in the WKYs and SHRs. On the other hand, dilatation of left ventricular end-diastolic dimension and impairment of left ventricular fractional shortening was shown only in salt loaded SHRs.
The high-salt diet markedly accelerated cardiac damage through the stimulation of cardiac (P)RR and angiotensin II AT1 receptor by increasing tissue prorenin, renin and angiotensinogen and the activation of ERK1/2, TGF-β, p38MAPK and HSP27 under higher blood pressure.</description><subject>Activation</subject><subject>Angiotensin AT1 receptors</subject><subject>Angiotensin II</subject><subject>Angiotensin II - blood</subject><subject>Angiotensinogen</subject><subject>Angiotensinogen - genetics</subject><subject>Angiotensinogen - metabolism</subject><subject>Angiotensins</subject><subject>Animals</subject><subject>Blood</subject><subject>Blood Pressure</subject><subject>Body Weight</subject><subject>Bone morphogenetic proteins</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Damage</subject><subject>Diet</subject><subject>Echocardiography</subject><subject>Fibrosis</subject><subject>Gene Expression</subject><subject>Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - metabolism</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart Ventricles - metabolism</subject><subject>Heart Ventricles - pathology</subject><subject>Heat shock proteins</subject><subject>HSP27 Heat-Shock Proteins - genetics</subject><subject>HSP27 Heat-Shock Proteins - metabolism</subject><subject>Hsp27 protein</subject><subject>Hypertension</subject><subject>Hypertension - etiology</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - pathology</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lung - pathology</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Myocardium</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Nutrition research</subject><subject>Organ Size</subject><subject>p38 Mitogen-Activated Protein Kinases - genetics</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Plasma</subject><subject>Prorenin Receptor</subject><subject>Rats</subject><subject>Receptor, Angiotensin, Type 1 - genetics</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Receptors</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Renin</subject><subject>Renin - blood</subject><subject>Renin - genetics</subject><subject>Rodents</subject><subject>Salts</subject><subject>Septum</subject><subject>Signal Transduction</subject><subject>Sodium Chloride, Dietary - administration & dosage</subject><subject>Sodium Chloride, Dietary - adverse effects</subject><subject>Transforming Growth Factor beta1 - genetics</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming growth factors</subject><subject>University graduates</subject><subject>Ventricle</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11r2zAUhs3YWLtu_2BsgsFoL5Lpy5J9MyhlWwOFwlZ2K05kOVHnSKkkh-Vi_31yk5Z49GIYZCE_73t0js8pircETwmT5NOt74ODbrr2zkwxoZiX7FlxTGpGJ4Ji9vxgf1S8ivEW45JVQrwsjmgp6xqL-rj4c2kXSxShS8i6BL8MamAFCxNRWhq0NBBS3gXfZwp0shtI1jvkW6QhNBY0Ol0Hf4aCcdblVZt18iEiszEOQULgUPbotiim7Droltu1Ccm4mH1eFy9a6KJ5s3-fFDdfv9xcXE6urr_NLs6vJlqWVZoQyQQIXnHe5ETbSnBoeDsHxmpaY6hoQwRhc2qM5rQpMSOCViDallKppWAnxfud7brzUe0LFxURQpIKV7TMxGxHNB5u1TrYFYSt8mDV_YEPC5UrYXVnFEiJMZdaSMAcA583pSw5nVeUGlLxIdrnfbR-vjKNNi4F6Eam4y_OLtXCbxRnEpeCZ4PTvUHwd72JSa1s1KbrwBnf399bSCokrjP64R_06ez21AJyAta1PsfVg6k655SWubLVEHb6BJWfxqyszl3W2nw-EpyNBJlJ5ndaQB-jmv34_v_s9c8x-_GAzT3YpWX0XT90XhyDfAfq4GMMpn0sMsFqGJKHaqhhSNR-SLLs3eEPehQ9TAX7C8BjC2c</recordid><startdate>20150323</startdate><enddate>20150323</enddate><creator>Hayakawa, Yuka</creator><creator>Aoyama, Takuma</creator><creator>Yokoyama, Chiharu</creator><creator>Okamoto, Chihiro</creator><creator>Komaki, Hisaaki</creator><creator>Minatoguchi, Shingo</creator><creator>Iwasa, Masamitsu</creator><creator>Yamada, Yoshihisa</creator><creator>Kawamura, Itta</creator><creator>Kawasaki, Masanori</creator><creator>Nishigaki, Kazuhiko</creator><creator>Mikami, Atsushi</creator><creator>Suzuki, Fumiaki</creator><creator>Minatoguchi, Shinya</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150323</creationdate><title>High salt intake damages the heart through activation of cardiac (pro) renin receptors even at an early stage of hypertension</title><author>Hayakawa, Yuka ; Aoyama, Takuma ; Yokoyama, Chiharu ; Okamoto, Chihiro ; Komaki, Hisaaki ; Minatoguchi, Shingo ; Iwasa, Masamitsu ; Yamada, Yoshihisa ; Kawamura, Itta ; Kawasaki, Masanori ; Nishigaki, Kazuhiko ; Mikami, Atsushi ; Suzuki, Fumiaki ; Minatoguchi, Shinya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-1736a64844d012f864ad4fba339290a82d1613b2eec42d5031628a6ff227c763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Activation</topic><topic>Angiotensin AT1 receptors</topic><topic>Angiotensin II</topic><topic>Angiotensin II - blood</topic><topic>Angiotensinogen</topic><topic>Angiotensinogen - genetics</topic><topic>Angiotensinogen - metabolism</topic><topic>Angiotensins</topic><topic>Animals</topic><topic>Blood</topic><topic>Blood Pressure</topic><topic>Body Weight</topic><topic>Bone morphogenetic proteins</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Damage</topic><topic>Diet</topic><topic>Echocardiography</topic><topic>Fibrosis</topic><topic>Gene Expression</topic><topic>Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - metabolism</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Heart Ventricles - metabolism</topic><topic>Heart Ventricles - pathology</topic><topic>Heat shock proteins</topic><topic>HSP27 Heat-Shock Proteins - genetics</topic><topic>HSP27 Heat-Shock Proteins - metabolism</topic><topic>Hsp27 protein</topic><topic>Hypertension</topic><topic>Hypertension - etiology</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - pathology</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lung - pathology</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Myocardium</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Nutrition research</topic><topic>Organ Size</topic><topic>p38 Mitogen-Activated Protein Kinases - genetics</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Plasma</topic><topic>Prorenin Receptor</topic><topic>Rats</topic><topic>Receptor, Angiotensin, Type 1 - genetics</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Receptors</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Renin</topic><topic>Renin - blood</topic><topic>Renin - genetics</topic><topic>Rodents</topic><topic>Salts</topic><topic>Septum</topic><topic>Signal Transduction</topic><topic>Sodium Chloride, Dietary - administration & dosage</topic><topic>Sodium Chloride, Dietary - adverse effects</topic><topic>Transforming Growth Factor beta1 - genetics</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Transforming growth factors</topic><topic>University graduates</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hayakawa, Yuka</creatorcontrib><creatorcontrib>Aoyama, Takuma</creatorcontrib><creatorcontrib>Yokoyama, Chiharu</creatorcontrib><creatorcontrib>Okamoto, Chihiro</creatorcontrib><creatorcontrib>Komaki, Hisaaki</creatorcontrib><creatorcontrib>Minatoguchi, Shingo</creatorcontrib><creatorcontrib>Iwasa, Masamitsu</creatorcontrib><creatorcontrib>Yamada, Yoshihisa</creatorcontrib><creatorcontrib>Kawamura, Itta</creatorcontrib><creatorcontrib>Kawasaki, Masanori</creatorcontrib><creatorcontrib>Nishigaki, Kazuhiko</creatorcontrib><creatorcontrib>Mikami, Atsushi</creatorcontrib><creatorcontrib>Suzuki, Fumiaki</creatorcontrib><creatorcontrib>Minatoguchi, Shinya</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale in Context : Opposing Viewpoints</collection><collection>Gale in Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>Biological Sciences</collection><collection>Agriculture Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>ProQuest Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hayakawa, Yuka</au><au>Aoyama, Takuma</au><au>Yokoyama, Chiharu</au><au>Okamoto, Chihiro</au><au>Komaki, Hisaaki</au><au>Minatoguchi, Shingo</au><au>Iwasa, Masamitsu</au><au>Yamada, Yoshihisa</au><au>Kawamura, Itta</au><au>Kawasaki, Masanori</au><au>Nishigaki, Kazuhiko</au><au>Mikami, Atsushi</au><au>Suzuki, Fumiaki</au><au>Minatoguchi, Shinya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High salt intake damages the heart through activation of cardiac (pro) renin receptors even at an early stage of hypertension</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-03-23</date><risdate>2015</risdate><volume>10</volume><issue>3</issue><spage>e0120453</spage><pages>e0120453-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>It has not yet been fully elucidated whether cardiac tissue levels of prorenin, renin and (P)RR are activated in hypertension with a high salt intake. We hypothesized that a high salt intake activates the cardiac tissue renin angiotensin system and prorenin-(pro)renin receptor system, and damages the heart at an early stage of hypertension.
Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) received regular (normal-salt diet, 0.9%) and high-salt (8.9%) chow for 6 weeks from 6 to 12 weeks of age. The systolic blood pressure, plasma renin activity (PRA) and plasma angiotensin II concentration were measured, and the protein expressions of prorenin, (pro)renin receptor, angiotensinogen, angiotensin II AT1 receptor, ERK1/2, TGF-β, p38MAPK and HSP27 in the myocardium were investigated. The cardiac function was assessed by echocardiography, and histological analysis of the myocardium was performed.
The high-salt diet significantly increased the systolic blood pressure, and significantly reduced the PRA and plasma angiotensin II concentration both in the WKYs and SHRs. Cardiac expressions of prorenin, renin, (P)RR, angiotensinogen, angiotensin II AT1 receptor, phosphorylated (p)-ERK1/2, p-p38MAPK, TGF-β and p-HSP27 were significantly increased by the high salt diet both in the WKYs and SHRs. The high-salt diet significantly increased the interventricular septum thickness and cardiomyocyte size, and accelerated cardiac interstitial and perivascular fibrosis both in the WKYs and SHRs. On the other hand, dilatation of left ventricular end-diastolic dimension and impairment of left ventricular fractional shortening was shown only in salt loaded SHRs.
The high-salt diet markedly accelerated cardiac damage through the stimulation of cardiac (P)RR and angiotensin II AT1 receptor by increasing tissue prorenin, renin and angiotensinogen and the activation of ERK1/2, TGF-β, p38MAPK and HSP27 under higher blood pressure.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25799069</pmid><doi>10.1371/journal.pone.0120453</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-03, Vol.10 (3), p.e0120453 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1667180825 |
| source | PLoS; MEDLINE; DOAJ Directory of Open Access Journals; PubMed Central; Free Full-Text Journals in Chemistry; EZB Electronic Journals Library |
| subjects | Activation Angiotensin AT1 receptors Angiotensin II Angiotensin II - blood Angiotensinogen Angiotensinogen - genetics Angiotensinogen - metabolism Angiotensins Animals Blood Blood Pressure Body Weight Bone morphogenetic proteins Cardiology Cardiomyocytes Damage Diet Echocardiography Fibrosis Gene Expression Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - metabolism Heart Heart diseases Heart Ventricles - metabolism Heart Ventricles - pathology Heat shock proteins HSP27 Heat-Shock Proteins - genetics HSP27 Heat-Shock Proteins - metabolism Hsp27 protein Hypertension Hypertension - etiology Hypertension - metabolism Hypertension - pathology Kidneys Kinases Laboratory animals Lung - pathology Male Medical research Medicine Myocardium Myocardium - metabolism Myocardium - pathology Nutrition research Organ Size p38 Mitogen-Activated Protein Kinases - genetics p38 Mitogen-Activated Protein Kinases - metabolism Plasma Prorenin Receptor Rats Receptor, Angiotensin, Type 1 - genetics Receptor, Angiotensin, Type 1 - metabolism Receptors Receptors, Cell Surface - genetics Receptors, Cell Surface - metabolism Renin Renin - blood Renin - genetics Rodents Salts Septum Signal Transduction Sodium Chloride, Dietary - administration & dosage Sodium Chloride, Dietary - adverse effects Transforming Growth Factor beta1 - genetics Transforming Growth Factor beta1 - metabolism Transforming growth factors University graduates Ventricle |
| title | High salt intake damages the heart through activation of cardiac (pro) renin receptors even at an early stage of hypertension |
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