Role of Aldosterone in Left Ventricular Hypertrophy in Hypertension
Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to inve...
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| Veröffentlicht in: | American journal of hypertension 2006, Vol.19 (1), p.13-18 |
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| description | Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients.
A total of 25 patients with primary aldosteronism caused by Conn’s adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects.
The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 ± 7.7, 142.3 ± 7.2, and 115.2 ± 7.2 g/m
2, respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism.
These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage. |
| doi_str_mv | 10.1016/j.amjhyper.2005.05.013 |
| format | Article |
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A total of 25 patients with primary aldosteronism caused by Conn’s adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects.
The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 ± 7.7, 142.3 ± 7.2, and 115.2 ± 7.2 g/m
2, respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism.
These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/j.amjhyper.2005.05.013</identifier><identifier>PMID: 16461184</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adrenergic beta-Antagonists - pharmacology ; Adrenergic beta-Antagonists - therapeutic use ; Adrenocortical Adenoma - complications ; Adrenocortical Adenoma - pathology ; Adrenocortical Adenoma - physiopathology ; Adult ; Aldosterone - physiology ; Angiotensin II - physiology ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Blood Pressure Monitoring, Ambulatory ; Calcium Channel Blockers - pharmacology ; Calcium Channel Blockers - therapeutic use ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Echocardiography ; Endomyocardial Fibrosis - pathology ; Endomyocardial Fibrosis - physiopathology ; Experimental diseases ; Female ; Heart Ventricles - pathology ; Heart Ventricles - physiopathology ; Humans ; Hyperaldosteronism - etiology ; Hyperaldosteronism - pathology ; Hyperaldosteronism - physiopathology ; Hypertension ; Hypertension - complications ; Hypertension - drug therapy ; Hypertension - physiopathology ; Hypertension, Renovascular - complications ; Hypertension, Renovascular - physiopathology ; Hypertrophy, Left Ventricular - etiology ; Hypertrophy, Left Ventricular - pathology ; Hypertrophy, Left Ventricular - physiopathology ; left ventricular hypertrophy ; Male ; Medical sciences ; Middle Aged ; primary aldosteronism ; Proteinuria - etiology ; Proteinuria - physiopathology ; Renin-Angiotensin System - physiology ; renovascular hypertension</subject><ispartof>American journal of hypertension, 2006, Vol.19 (1), p.13-18</ispartof><rights>2006 American Journal of Hypertension, Ltd.</rights><rights>2006 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-a975860ffd38f6a5c705f02c92d7aad3080bd666e4f51c4e0c96c43a2f3d3b7f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4021,27921,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17747766$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16461184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsumura, Kiyoshi</creatorcontrib><creatorcontrib>Fujii, Koji</creatorcontrib><creatorcontrib>Oniki, Hideyuki</creatorcontrib><creatorcontrib>Oka, Masayo</creatorcontrib><creatorcontrib>Iida, Mitsuo</creatorcontrib><title>Role of Aldosterone in Left Ventricular Hypertrophy in Hypertension</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients.
A total of 25 patients with primary aldosteronism caused by Conn’s adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects.
The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 ± 7.7, 142.3 ± 7.2, and 115.2 ± 7.2 g/m
2, respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism.
These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.</description><subject>Adrenergic beta-Antagonists - pharmacology</subject><subject>Adrenergic beta-Antagonists - therapeutic use</subject><subject>Adrenocortical Adenoma - complications</subject><subject>Adrenocortical Adenoma - pathology</subject><subject>Adrenocortical Adenoma - physiopathology</subject><subject>Adult</subject><subject>Aldosterone - physiology</subject><subject>Angiotensin II - physiology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Blood Pressure Monitoring, Ambulatory</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channel Blockers - therapeutic use</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Echocardiography</subject><subject>Endomyocardial Fibrosis - pathology</subject><subject>Endomyocardial Fibrosis - physiopathology</subject><subject>Experimental diseases</subject><subject>Female</subject><subject>Heart Ventricles - pathology</subject><subject>Heart Ventricles - physiopathology</subject><subject>Humans</subject><subject>Hyperaldosteronism - etiology</subject><subject>Hyperaldosteronism - pathology</subject><subject>Hyperaldosteronism - physiopathology</subject><subject>Hypertension</subject><subject>Hypertension - complications</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Hypertension, Renovascular - complications</subject><subject>Hypertension, Renovascular - physiopathology</subject><subject>Hypertrophy, Left Ventricular - etiology</subject><subject>Hypertrophy, Left Ventricular - pathology</subject><subject>Hypertrophy, Left Ventricular - physiopathology</subject><subject>left ventricular hypertrophy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>primary aldosteronism</subject><subject>Proteinuria - etiology</subject><subject>Proteinuria - physiopathology</subject><subject>Renin-Angiotensin System - physiology</subject><subject>renovascular hypertension</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkV2rEzEQhoMonnr0LxwWRO-2Jpuv3TsPxXMqVKyiIt6ENDuhWbdJTXbF_nuzbLXgjTAQwjzzzsw7CN0QvCSYiFfdUh-6_ekIcVlhzJdTEPoALUgtm5I0mD9EC1w3vJRYkCv0JKUOY8yEII_RFRFMEFKzBVp9DD0UwRa3fRvSADF4KJwvNmCH4gv4IToz9joW66nXEMNxf5ry8xd8csE_RY-s7hM8O7_X6PPdm0-rdbl5f_92dbspDad0KHUjeS2wtS2trdDcSMwtrkxTtVLrluIa71ohBDDLiWGATSMMo7qytKU7aek1ejnrHmP4MUIa1MElA32vPYQxKSEFlYRXGXz-D9iFMfo8myK44pJRzppMiZkyMaQUwapjdAcdTxlSk8mqU39MVpPJagpCc-HNWX7cHaC9lJ1dzcCLM6CT0b2N2huXLpyUTEohLkJeD2OEv4Du9rmfmITKGXD5NL8u-fg9L0slV-uv39T9HeXbD--2apv51zMP-Qw_XZ47GQfeQOsimEG1wf1vud9i1rdJ</recordid><startdate>2006</startdate><enddate>2006</enddate><creator>Matsumura, Kiyoshi</creator><creator>Fujii, Koji</creator><creator>Oniki, Hideyuki</creator><creator>Oka, Masayo</creator><creator>Iida, Mitsuo</creator><general>Elsevier Inc</general><general>Oxford University Press</general><general>Elsevier Science</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>2006</creationdate><title>Role of Aldosterone in Left Ventricular Hypertrophy in Hypertension</title><author>Matsumura, Kiyoshi ; Fujii, Koji ; Oniki, Hideyuki ; Oka, Masayo ; Iida, Mitsuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-a975860ffd38f6a5c705f02c92d7aad3080bd666e4f51c4e0c96c43a2f3d3b7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adrenergic beta-Antagonists - pharmacology</topic><topic>Adrenergic beta-Antagonists - therapeutic use</topic><topic>Adrenocortical Adenoma - complications</topic><topic>Adrenocortical Adenoma - pathology</topic><topic>Adrenocortical Adenoma - physiopathology</topic><topic>Adult</topic><topic>Aldosterone - physiology</topic><topic>Angiotensin II - physiology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Blood Pressure Monitoring, Ambulatory</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channel Blockers - therapeutic use</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Echocardiography</topic><topic>Endomyocardial Fibrosis - pathology</topic><topic>Endomyocardial Fibrosis - physiopathology</topic><topic>Experimental diseases</topic><topic>Female</topic><topic>Heart Ventricles - pathology</topic><topic>Heart Ventricles - physiopathology</topic><topic>Humans</topic><topic>Hyperaldosteronism - etiology</topic><topic>Hyperaldosteronism - pathology</topic><topic>Hyperaldosteronism - physiopathology</topic><topic>Hypertension</topic><topic>Hypertension - complications</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - physiopathology</topic><topic>Hypertension, Renovascular - complications</topic><topic>Hypertension, Renovascular - physiopathology</topic><topic>Hypertrophy, Left Ventricular - etiology</topic><topic>Hypertrophy, Left Ventricular - pathology</topic><topic>Hypertrophy, Left Ventricular - physiopathology</topic><topic>left ventricular hypertrophy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>primary aldosteronism</topic><topic>Proteinuria - etiology</topic><topic>Proteinuria - physiopathology</topic><topic>Renin-Angiotensin System - physiology</topic><topic>renovascular hypertension</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsumura, Kiyoshi</creatorcontrib><creatorcontrib>Fujii, Koji</creatorcontrib><creatorcontrib>Oniki, Hideyuki</creatorcontrib><creatorcontrib>Oka, Masayo</creatorcontrib><creatorcontrib>Iida, Mitsuo</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsumura, Kiyoshi</au><au>Fujii, Koji</au><au>Oniki, Hideyuki</au><au>Oka, Masayo</au><au>Iida, Mitsuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Aldosterone in Left Ventricular Hypertrophy in Hypertension</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2006</date><risdate>2006</risdate><volume>19</volume><issue>1</issue><spage>13</spage><epage>18</epage><pages>13-18</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients.
A total of 25 patients with primary aldosteronism caused by Conn’s adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects.
The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 ± 7.7, 142.3 ± 7.2, and 115.2 ± 7.2 g/m
2, respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism.
These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>16461184</pmid><doi>10.1016/j.amjhyper.2005.05.013</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | American journal of hypertension, 2006, Vol.19 (1), p.13-18 |
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| subjects | Adrenergic beta-Antagonists - pharmacology Adrenergic beta-Antagonists - therapeutic use Adrenocortical Adenoma - complications Adrenocortical Adenoma - pathology Adrenocortical Adenoma - physiopathology Adult Aldosterone - physiology Angiotensin II - physiology Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure - drug effects Blood Pressure - physiology Blood Pressure Monitoring, Ambulatory Calcium Channel Blockers - pharmacology Calcium Channel Blockers - therapeutic use Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Echocardiography Endomyocardial Fibrosis - pathology Endomyocardial Fibrosis - physiopathology Experimental diseases Female Heart Ventricles - pathology Heart Ventricles - physiopathology Humans Hyperaldosteronism - etiology Hyperaldosteronism - pathology Hyperaldosteronism - physiopathology Hypertension Hypertension - complications Hypertension - drug therapy Hypertension - physiopathology Hypertension, Renovascular - complications Hypertension, Renovascular - physiopathology Hypertrophy, Left Ventricular - etiology Hypertrophy, Left Ventricular - pathology Hypertrophy, Left Ventricular - physiopathology left ventricular hypertrophy Male Medical sciences Middle Aged primary aldosteronism Proteinuria - etiology Proteinuria - physiopathology Renin-Angiotensin System - physiology renovascular hypertension |
| title | Role of Aldosterone in Left Ventricular Hypertrophy in Hypertension |
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