Renin–angiotensin system and fibronectin gene expression in Dahl Iwai salt-sensitive and salt-resistant rats
OBJECTIVEThe tissue renin–angiotensin system and extracellular matrix are involved in the cardiovascular hypertrophy and remodeling induced by hypertension. In this study, we examined the gene expression of the tissue renin–angiotensin system and fibronectin in inbred Dahl Iwai salt-sensitive and sa...
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creator | Tamura, Kouichi Chiba, Eiko Yokoyama, Nobuyuki Sumida, Yoichi Yabana, Machiko Tamura, Nobuko Takasaki, Izumi Takagi, Nobuyoshi Ishii, Masao Horiuchi, Masatsugu Umemura, Satoshi |
description | OBJECTIVEThe tissue renin–angiotensin system and extracellular matrix are involved in the cardiovascular hypertrophy and remodeling induced by hypertension. In this study, we examined the gene expression of the tissue renin–angiotensin system and fibronectin in inbred Dahl Iwai salt-sensitive and salt-resistant rats.
MATERIALS AND METHODSEight pairs of 6-week-old male Dahl Iwai salt-sensitive and salt-resistant rats were fed either a low- or high-salt diet (0.3% or 8% NaCl, respectively) for 4 weeks. Activities of the circulating renin–angiotensin system were measured by radioimmunoassay and the gene expression of tissue angiotensinogen, the angiotensin II type 1 receptor (AT1) and fibronectin were analyzed by Northern blot analysis.
RESULTSSalt loading significantly increased blood pressure and produced cardiovascular hypertrophy and nephrosclerosis in the salt-sensitive rats. Activities of the circulating renin–angiotensin system were lower in salt-sensitive rats than in salt-resistant rats fed the low-salt diet, and salt loading lowered these activities in salt-resistant rats but not in salt-sensitive rats. In salt-resistant rats, salt loading increased renal, cardiac and aortic angiotensinogen, AT1 and fibronectin messenger (m)RNA expression except for aortic fibronectin mRNA expression. In contrast, in the salt-sensitive rats, salt loading stimulated the expression of cardiac fibronectin and aortic angiotensinogen, AT1 and fibronectin mRNAs. Furthermore, the cardiac and aortic fibronectin mRNA levels in salt-sensitive rats were higher than those in salt-resistant rats when both strains were fed the high-salt diet.
CONCLUSIONSThese results demonstrate that the expression of tissue angiotensinogen, AT1 and fibronectin mRNAs is regulated differently in Dahl Iwai salt-sensitive and salt-resistant rats, and indicate that salt-mediated hypertension activates the cardiac fibronectin gene independently of the tissue renin–angiotensin system and stimulates the aortic fibronectin gene with activation of the tissue renin–angiotensin system. |
doi_str_mv | 10.1097/00004872-199917010-00013 |
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MATERIALS AND METHODSEight pairs of 6-week-old male Dahl Iwai salt-sensitive and salt-resistant rats were fed either a low- or high-salt diet (0.3% or 8% NaCl, respectively) for 4 weeks. Activities of the circulating renin–angiotensin system were measured by radioimmunoassay and the gene expression of tissue angiotensinogen, the angiotensin II type 1 receptor (AT1) and fibronectin were analyzed by Northern blot analysis.
RESULTSSalt loading significantly increased blood pressure and produced cardiovascular hypertrophy and nephrosclerosis in the salt-sensitive rats. Activities of the circulating renin–angiotensin system were lower in salt-sensitive rats than in salt-resistant rats fed the low-salt diet, and salt loading lowered these activities in salt-resistant rats but not in salt-sensitive rats. In salt-resistant rats, salt loading increased renal, cardiac and aortic angiotensinogen, AT1 and fibronectin messenger (m)RNA expression except for aortic fibronectin mRNA expression. In contrast, in the salt-sensitive rats, salt loading stimulated the expression of cardiac fibronectin and aortic angiotensinogen, AT1 and fibronectin mRNAs. Furthermore, the cardiac and aortic fibronectin mRNA levels in salt-sensitive rats were higher than those in salt-resistant rats when both strains were fed the high-salt diet.
CONCLUSIONSThese results demonstrate that the expression of tissue angiotensinogen, AT1 and fibronectin mRNAs is regulated differently in Dahl Iwai salt-sensitive and salt-resistant rats, and indicate that salt-mediated hypertension activates the cardiac fibronectin gene independently of the tissue renin–angiotensin system and stimulates the aortic fibronectin gene with activation of the tissue renin–angiotensin system.</description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/00004872-199917010-00013</identifier><identifier>PMID: 10100098</identifier><identifier>CODEN: JOHYD3</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Angiotensin I - genetics ; Angiotensinogen - genetics ; Animals ; Aorta, Thoracic - metabolism ; Aorta, Thoracic - pathology ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Blotting, Northern ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Fibronectins - genetics ; Gene Expression ; Hypertension - genetics ; Hypertension - metabolism ; Hypertension - pathology ; Male ; Medical sciences ; Myocardium - metabolism ; Myocardium - pathology ; Radioimmunoassay ; Rats ; Rats, Inbred Dahl ; Receptor, Angiotensin, Type 1 ; Receptor, Angiotensin, Type 2 ; Receptors, Angiotensin - genetics ; Renin-Angiotensin System - genetics ; RNA, Messenger - biosynthesis ; Sodium, Dietary - administration & dosage</subject><ispartof>Journal of hypertension, 1999-01, Vol.17 (1), p.81-89</ispartof><rights>1999 Lippincott Williams & Wilkins, Inc.</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4513-805eeed53d105a049c17bbab48eff3e7c2bcbf9cca4fb79146da2caa9eb666a53</citedby><cites>FETCH-LOGICAL-c4513-805eeed53d105a049c17bbab48eff3e7c2bcbf9cca4fb79146da2caa9eb666a53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1689792$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10100098$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tamura, Kouichi</creatorcontrib><creatorcontrib>Chiba, Eiko</creatorcontrib><creatorcontrib>Yokoyama, Nobuyuki</creatorcontrib><creatorcontrib>Sumida, Yoichi</creatorcontrib><creatorcontrib>Yabana, Machiko</creatorcontrib><creatorcontrib>Tamura, Nobuko</creatorcontrib><creatorcontrib>Takasaki, Izumi</creatorcontrib><creatorcontrib>Takagi, Nobuyoshi</creatorcontrib><creatorcontrib>Ishii, Masao</creatorcontrib><creatorcontrib>Horiuchi, Masatsugu</creatorcontrib><creatorcontrib>Umemura, Satoshi</creatorcontrib><title>Renin–angiotensin system and fibronectin gene expression in Dahl Iwai salt-sensitive and salt-resistant rats</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>OBJECTIVEThe tissue renin–angiotensin system and extracellular matrix are involved in the cardiovascular hypertrophy and remodeling induced by hypertension. In this study, we examined the gene expression of the tissue renin–angiotensin system and fibronectin in inbred Dahl Iwai salt-sensitive and salt-resistant rats.
MATERIALS AND METHODSEight pairs of 6-week-old male Dahl Iwai salt-sensitive and salt-resistant rats were fed either a low- or high-salt diet (0.3% or 8% NaCl, respectively) for 4 weeks. Activities of the circulating renin–angiotensin system were measured by radioimmunoassay and the gene expression of tissue angiotensinogen, the angiotensin II type 1 receptor (AT1) and fibronectin were analyzed by Northern blot analysis.
RESULTSSalt loading significantly increased blood pressure and produced cardiovascular hypertrophy and nephrosclerosis in the salt-sensitive rats. Activities of the circulating renin–angiotensin system were lower in salt-sensitive rats than in salt-resistant rats fed the low-salt diet, and salt loading lowered these activities in salt-resistant rats but not in salt-sensitive rats. In salt-resistant rats, salt loading increased renal, cardiac and aortic angiotensinogen, AT1 and fibronectin messenger (m)RNA expression except for aortic fibronectin mRNA expression. In contrast, in the salt-sensitive rats, salt loading stimulated the expression of cardiac fibronectin and aortic angiotensinogen, AT1 and fibronectin mRNAs. Furthermore, the cardiac and aortic fibronectin mRNA levels in salt-sensitive rats were higher than those in salt-resistant rats when both strains were fed the high-salt diet.
CONCLUSIONSThese results demonstrate that the expression of tissue angiotensinogen, AT1 and fibronectin mRNAs is regulated differently in Dahl Iwai salt-sensitive and salt-resistant rats, and indicate that salt-mediated hypertension activates the cardiac fibronectin gene independently of the tissue renin–angiotensin system and stimulates the aortic fibronectin gene with activation of the tissue renin–angiotensin system.</description><subject>Angiotensin I - genetics</subject><subject>Angiotensinogen - genetics</subject><subject>Animals</subject><subject>Aorta, Thoracic - metabolism</subject><subject>Aorta, Thoracic - pathology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Blotting, Northern</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Fibronectins - genetics</subject><subject>Gene Expression</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Radioimmunoassay</subject><subject>Rats</subject><subject>Rats, Inbred Dahl</subject><subject>Receptor, Angiotensin, Type 1</subject><subject>Receptor, Angiotensin, Type 2</subject><subject>Receptors, Angiotensin - genetics</subject><subject>Renin-Angiotensin System - genetics</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Sodium, Dietary - administration & dosage</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9u1DAQh60K1C6FV0A-IG4BO06c-FiVf5UqISE4W2Nn0jXNOluPl6U33oE35Enq7m4pF3wZ6afvN5a-YYxL8UYK070V5TV9V1fSGCM7IUVVEqmO2EI2nara1vRP2ELUWlVatfUJe0b0vSC96dQxO5GlIYTpFyx-wRjin1-_IV6FOWOkEDndUsYVhzjwMbg0R_S5xFcYkePPdUKiMEdeonewnPjFFgInmHJF9_0cfuCuu4sKHChDzDxBpufs6QgT4YvDPGXfPrz_ev6puvz88eL87LLyTStV1YsWEYdWDVK0IBrjZeccuKbHcVTY-dp5NxrvoRldZ2SjB6g9gEGntYZWnbLX-73rNN9skLJdBfI4TRBx3pDVRutamb6A_R70aSZKONp1CitIt1YKe-_aPri2f13bnetSfXn4Y-NWOPxT3MstwKsDAORhGhNEH-iR0-Uapi5Ys8e285Qx0fW02WKySyz6lvZ_p1Z3No6aWA</recordid><startdate>199901</startdate><enddate>199901</enddate><creator>Tamura, Kouichi</creator><creator>Chiba, Eiko</creator><creator>Yokoyama, Nobuyuki</creator><creator>Sumida, Yoichi</creator><creator>Yabana, Machiko</creator><creator>Tamura, Nobuko</creator><creator>Takasaki, Izumi</creator><creator>Takagi, Nobuyoshi</creator><creator>Ishii, Masao</creator><creator>Horiuchi, Masatsugu</creator><creator>Umemura, Satoshi</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199901</creationdate><title>Renin–angiotensin system and fibronectin gene expression in Dahl Iwai salt-sensitive and salt-resistant rats</title><author>Tamura, Kouichi ; Chiba, Eiko ; Yokoyama, Nobuyuki ; Sumida, Yoichi ; Yabana, Machiko ; Tamura, Nobuko ; Takasaki, Izumi ; Takagi, Nobuyoshi ; Ishii, Masao ; Horiuchi, Masatsugu ; Umemura, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4513-805eeed53d105a049c17bbab48eff3e7c2bcbf9cca4fb79146da2caa9eb666a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Angiotensin I - genetics</topic><topic>Angiotensinogen - genetics</topic><topic>Animals</topic><topic>Aorta, Thoracic - metabolism</topic><topic>Aorta, Thoracic - pathology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Blotting, Northern</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Fibronectins - genetics</topic><topic>Gene Expression</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Radioimmunoassay</topic><topic>Rats</topic><topic>Rats, Inbred Dahl</topic><topic>Receptor, Angiotensin, Type 1</topic><topic>Receptor, Angiotensin, Type 2</topic><topic>Receptors, Angiotensin - genetics</topic><topic>Renin-Angiotensin System - genetics</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Sodium, Dietary - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tamura, Kouichi</creatorcontrib><creatorcontrib>Chiba, Eiko</creatorcontrib><creatorcontrib>Yokoyama, Nobuyuki</creatorcontrib><creatorcontrib>Sumida, Yoichi</creatorcontrib><creatorcontrib>Yabana, Machiko</creatorcontrib><creatorcontrib>Tamura, Nobuko</creatorcontrib><creatorcontrib>Takasaki, Izumi</creatorcontrib><creatorcontrib>Takagi, Nobuyoshi</creatorcontrib><creatorcontrib>Ishii, Masao</creatorcontrib><creatorcontrib>Horiuchi, Masatsugu</creatorcontrib><creatorcontrib>Umemura, Satoshi</creatorcontrib><collection>Pascal-Francis</collection><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><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tamura, Kouichi</au><au>Chiba, Eiko</au><au>Yokoyama, Nobuyuki</au><au>Sumida, Yoichi</au><au>Yabana, Machiko</au><au>Tamura, Nobuko</au><au>Takasaki, Izumi</au><au>Takagi, Nobuyoshi</au><au>Ishii, Masao</au><au>Horiuchi, Masatsugu</au><au>Umemura, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renin–angiotensin system and fibronectin gene expression in Dahl Iwai salt-sensitive and salt-resistant rats</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>1999-01</date><risdate>1999</risdate><volume>17</volume><issue>1</issue><spage>81</spage><epage>89</epage><pages>81-89</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><coden>JOHYD3</coden><abstract>OBJECTIVEThe tissue renin–angiotensin system and extracellular matrix are involved in the cardiovascular hypertrophy and remodeling induced by hypertension. In this study, we examined the gene expression of the tissue renin–angiotensin system and fibronectin in inbred Dahl Iwai salt-sensitive and salt-resistant rats.
MATERIALS AND METHODSEight pairs of 6-week-old male Dahl Iwai salt-sensitive and salt-resistant rats were fed either a low- or high-salt diet (0.3% or 8% NaCl, respectively) for 4 weeks. Activities of the circulating renin–angiotensin system were measured by radioimmunoassay and the gene expression of tissue angiotensinogen, the angiotensin II type 1 receptor (AT1) and fibronectin were analyzed by Northern blot analysis.
RESULTSSalt loading significantly increased blood pressure and produced cardiovascular hypertrophy and nephrosclerosis in the salt-sensitive rats. Activities of the circulating renin–angiotensin system were lower in salt-sensitive rats than in salt-resistant rats fed the low-salt diet, and salt loading lowered these activities in salt-resistant rats but not in salt-sensitive rats. In salt-resistant rats, salt loading increased renal, cardiac and aortic angiotensinogen, AT1 and fibronectin messenger (m)RNA expression except for aortic fibronectin mRNA expression. In contrast, in the salt-sensitive rats, salt loading stimulated the expression of cardiac fibronectin and aortic angiotensinogen, AT1 and fibronectin mRNAs. Furthermore, the cardiac and aortic fibronectin mRNA levels in salt-sensitive rats were higher than those in salt-resistant rats when both strains were fed the high-salt diet.
CONCLUSIONSThese results demonstrate that the expression of tissue angiotensinogen, AT1 and fibronectin mRNAs is regulated differently in Dahl Iwai salt-sensitive and salt-resistant rats, and indicate that salt-mediated hypertension activates the cardiac fibronectin gene independently of the tissue renin–angiotensin system and stimulates the aortic fibronectin gene with activation of the tissue renin–angiotensin system.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>10100098</pmid><doi>10.1097/00004872-199917010-00013</doi><tpages>9</tpages></addata></record> |
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subjects | Angiotensin I - genetics Angiotensinogen - genetics Animals Aorta, Thoracic - metabolism Aorta, Thoracic - pathology Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure Blotting, Northern Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Fibronectins - genetics Gene Expression Hypertension - genetics Hypertension - metabolism Hypertension - pathology Male Medical sciences Myocardium - metabolism Myocardium - pathology Radioimmunoassay Rats Rats, Inbred Dahl Receptor, Angiotensin, Type 1 Receptor, Angiotensin, Type 2 Receptors, Angiotensin - genetics Renin-Angiotensin System - genetics RNA, Messenger - biosynthesis Sodium, Dietary - administration & dosage |
title | Renin–angiotensin system and fibronectin gene expression in Dahl Iwai salt-sensitive and salt-resistant rats |
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