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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| Published in: | PloS one Vol. 10; no. 3; p. e0120453 |
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| Main Authors: | , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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23-03-2015
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| 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. |
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| AbstractList | 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. Objective 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. Methods 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. Results 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. Conclusion 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. 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. 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-[beta], 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-[beta] 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-[beta], p38MAPK and HSP27 under higher blood pressure. Objective 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. Methods 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. Results 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. Conclusion 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. Objective 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. Methods 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-[beta], p38MAPK and HSP27 in the myocardium were investigated. The cardiac function was assessed by echocardiography, and histological analysis of the myocardium was performed. Results 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-[beta] 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. Conclusion 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-[beta], p38MAPK and HSP27 under higher blood pressure. 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.OBJECTIVEIt 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.METHODSWistar 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.RESULTSThe 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.CONCLUSIONThe 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. |
| Audience | Academic |
| Author | Aoyama, Takuma Kawamura, Itta Suzuki, Fumiaki Okamoto, Chihiro Nishigaki, Kazuhiko Yamada, Yoshihisa Yokoyama, Chiharu Minatoguchi, Shingo Minatoguchi, Shinya Kawasaki, Masanori Hayakawa, Yuka Iwasa, Masamitsu Mikami, Atsushi Komaki, Hisaaki |
| AuthorAffiliation | 1 Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan Universidade Federal do Rio de Janeiro, BRAZIL 2 Department of Life Science, Gifu University, Yanagido, Gifu, Japan |
| AuthorAffiliation_xml | – name: 1 Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – name: 2 Department of Life Science, Gifu University, Yanagido, Gifu, Japan – name: Universidade Federal do Rio de Janeiro, BRAZIL |
| Author_xml | – sequence: 1 givenname: Yuka surname: Hayakawa fullname: Hayakawa, Yuka organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 2 givenname: Takuma surname: Aoyama fullname: Aoyama, Takuma organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 3 givenname: Chiharu surname: Yokoyama fullname: Yokoyama, Chiharu organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 4 givenname: Chihiro surname: Okamoto fullname: Okamoto, Chihiro organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 5 givenname: Hisaaki surname: Komaki fullname: Komaki, Hisaaki organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 6 givenname: Shingo surname: Minatoguchi fullname: Minatoguchi, Shingo organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 7 givenname: Masamitsu surname: Iwasa fullname: Iwasa, Masamitsu organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 8 givenname: Yoshihisa surname: Yamada fullname: Yamada, Yoshihisa organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 9 givenname: Itta surname: Kawamura fullname: Kawamura, Itta organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 10 givenname: Masanori surname: Kawasaki fullname: Kawasaki, Masanori organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 11 givenname: Kazuhiko surname: Nishigaki fullname: Nishigaki, Kazuhiko organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 12 givenname: Atsushi surname: Mikami fullname: Mikami, Atsushi organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan – sequence: 13 givenname: Fumiaki surname: Suzuki fullname: Suzuki, Fumiaki organization: Department of Life Science, Gifu University, Yanagido, Gifu, Japan – sequence: 14 givenname: Shinya surname: Minatoguchi fullname: Minatoguchi, Shinya organization: Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25799069$$D View this record in MEDLINE/PubMed |
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| Copyright | COPYRIGHT 2015 Public Library of Science 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. 2015 Hayakawa et al 2015 Hayakawa et al |
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| DOI | 10.1371/journal.pone.0120453 |
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| Discipline | Sciences (General) Medicine |
| DocumentTitleAlternate | Salt Activates Cardiac Prorenin Receptors |
| EISSN | 1932-6203 |
| Editor | Quintas, Luis Eduardo M |
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| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Competing Interests: The authors have declared that no competing interest exist. Conceived and designed the experiments: SM TA. Performed the experiments: YH CY HK SM. Analyzed the data: MK KN FS. Contributed reagents/materials/analysis tools: CO MI YY IK AM. Wrote the paper: SM YH. |
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| References | A Ichihara (ref5) 2004; 114 John E Hall (ref15) 2011 J Schnermann (ref3) 2008 D Susic (ref6) 2008; 295 DN Ferreira (ref11) 2010; 140 AH Dunser (ref25) 2005; 46 DA Price (ref9) 1999; 10 A Ichihara (ref21) 2006; 47 U Danilczyk (ref16) 2004; 10 MG Morales (ref24) 2012; 44 SB Gurley (ref10) 2007; 27 W Li (ref17) 2014; 63 D Denton (ref8) 1995; 1 IA Katayama (ref12) 2014; 144 K Fujii (ref13) 1999; 22 M Sakoda (ref20) 2007; 30 JJ Saris (ref23) 2006; 48 AB Ribeiro (ref1) 1985; 30 Y Huang (ref19) 2007; 72 G Hodge (ref7) 2002; 174 JJ Kang (ref4) 2008; 51 NF Schroten (ref22) 2012; 17 MS Coelho (ref18) 2006; 16 J Varagic (ref14) 2006; 290 V Gerc (ref2) 2010; 64 |
| References_xml | – volume: 72 start-page: 45 year: 2007 ident: ref19 article-title: Renin-stimulated TGF-beta1 expression is regulated by a mitogen-activated protein kinase in mesangial cells publication-title: Kidney Int doi: 10.1038/sj.ki.5002243 contributor: fullname: Y Huang – volume: 47 start-page: 894 year: 2006 ident: ref21 article-title: Nonproteolytic activation of prorenin contributes to development of cardiac fibrosis in genetic hypertension publication-title: Hypertension doi: 10.1161/01.HYP.0000215838.48170.0b contributor: fullname: A Ichihara – volume: 63 start-page: 316 year: 2014 ident: ref17 article-title: Neuron-specific (pro)renin receptor knockout prevents the development of salt-sensitive hypertension publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.113.02041 contributor: fullname: W Li – volume: 17 start-page: 191 year: 2012 ident: ref22 article-title: New roles for renin and prorenin in heart failure and cardiorenal crosstalk publication-title: Heart Fail Rev doi: 10.1007/s10741-011-9262-2 contributor: fullname: NF Schroten – start-page: 589 year: 2008 ident: ref3 article-title: The Kidney Physiology and Pathophysiology contributor: fullname: J Schnermann – volume: 10 start-page: 2382 year: 1999 ident: ref9 article-title: The paradox of the low-renin state in diabetic nephropathy publication-title: J Am Soc Nephrol doi: 10.1681/ASN.V10112382 contributor: fullname: DA Price – volume: 16 start-page: 148 year: 2006 ident: ref18 article-title: High- or low-salt diet from weaning to adulthood: Effect on body weight, food intake and energy balance in rats publication-title: Nutrition, Metabolism & Cardiovascular Disease doi: 10.1016/j.numecd.2005.09.001 contributor: fullname: MS Coelho – volume: 30 start-page: 6 issue: Suppl 1 year: 1985 ident: ref1 article-title: The renin-angiotensin system in the control of systemic arterial pressure publication-title: Drugs doi: 10.2165/00003495-198500301-00003 contributor: fullname: AB Ribeiro – volume: 48 start-page: 564 year: 2006 ident: ref23 article-title: Prorenin induces intracellular signaling in cardiomyocytes independently of angiotensin II publication-title: Hypertension doi: 10.1161/01.HYP.0000240064.19301.1b contributor: fullname: JJ Saris – volume: 64 start-page: 295 year: 2010 ident: ref2 article-title: Advantages of renin-angiotensin system blockade in the treatment of cardiovascular diseases publication-title: Med Arh contributor: fullname: V Gerc – volume: 10 start-page: 1193 year: 2004 ident: ref16 article-title: Hypertension with a grant of salt publication-title: Nat Med doi: 10.1038/nm1104-1163 contributor: fullname: U Danilczyk – volume: 44 start-page: 1993 year: 2012 ident: ref24 article-title: Angiotensin II-induced pro-fibrotic effects require p38MAPK activity and transforming growth factor beta 1 expression in skeletal muscle cells publication-title: Int J Biochem Cell Biol doi: 10.1016/j.biocel.2012.07.028 contributor: fullname: MG Morales – volume: 46 start-page: 1069 year: 2005 ident: ref25 article-title: Renin, prorenin and the putative (pro)renin receptor publication-title: Hypertension doi: 10.1161/01.HYP.0000186329.92187.2e contributor: fullname: AH Dunser – volume: 114 start-page: 1128 year: 2004 ident: ref5 article-title: Inhibition of diabetic nephropathy by a decoy peptide corresponding to the ‘handle’ region for nonproteolytic activation of prorenin publication-title: J Clin Invest doi: 10.1172/JCI21398 contributor: fullname: A Ichihara – volume: 140 start-page: 1742 year: 2010 ident: ref11 article-title: Salt-induced cardiac hypertrophy and interstitial fibrosis are due to a blood pressure-independent mechanism in wistar rats publication-title: J Nutr doi: 10.3945/jn.109.117473 contributor: fullname: DN Ferreira – volume: 290 start-page: H1503 year: 2006 ident: ref14 article-title: Myocardial fibrosis, impaired coronary hemodynamics, and biventricular dysfunction in salt-loaded SHR publication-title: Am J Physiol. Heart and Circulatory Physiol doi: 10.1152/ajpheart.00970.2005 contributor: fullname: J Varagic – volume: 51 start-page: 1597 year: 2008 ident: ref4 article-title: The collecting duct is the major source of prorenin in diabetes publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.107.107268 contributor: fullname: JJ Kang – volume: 295 start-page: H1117 year: 2008 ident: ref6 article-title: Cardiovascular effects of prorenin blockade in genetically spontaneously hypertensive rats on normal and high-salt diet publication-title: Am J Physiol Heart Circ Physiol doi: 10.1152/ajpheart.00055.2008 contributor: fullname: D Susic – volume: 30 start-page: 1139 year: 2007 ident: ref20 article-title: (Pro)renin receptor-mediated activation of mitogen-activated protein kinases in human vascular smooth muscle cells publication-title: Hypertens Res doi: 10.1291/hypres.30.1139 contributor: fullname: M Sakoda – volume: 144 start-page: 1571 year: 2014 ident: ref12 article-title: High-Salt Intake Induces Cardiomyocyte Hypertrophy in Rats in Response to Local Angiotensin II Type 1 Receptor Activation publication-title: J Nutr doi: 10.3945/jn.114.192054 contributor: fullname: IA Katayama – volume: 22 start-page: 181 year: 1999 ident: ref13 article-title: Effects of salt-loading on membrane potentials in mesenteric arteries of spontaneously hypertensive rats publication-title: Hypertens Res doi: 10.1291/hypres.22.181 contributor: fullname: K Fujii – volume: 174 start-page: 209 year: 2002 ident: ref7 article-title: Dysregulation of angiotensin II synthesis is associated with salt sensitivity in the spontaneous hypertensive rat publication-title: Acta Physiol Scand doi: 10.1046/j.1365-201x.2002.00937.x contributor: fullname: G Hodge – volume: 27 start-page: 144 year: 2007 ident: ref10 article-title: The renin-angiotensin system and diabetic nephropathy publication-title: Semin Nephrol doi: 10.1016/j.semnephrol.2007.01.009 contributor: fullname: SB Gurley – volume: 1 start-page: 1009 year: 1995 ident: ref8 article-title: The effect of increased salt intake on blood pressure of chimpanzees publication-title: Nat Med doi: 10.1038/nm1095-1009 contributor: fullname: D Denton – start-page: 213 year: 2011 ident: ref15 article-title: Guyton and Hall Textbook of Medical Physiology TWELFTH EDITION contributor: fullname: John E Hall |
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| Snippet | 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... Objective 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... Objective 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... |
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| SubjectTerms | 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 |
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| 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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