Mineralocorticoid Signaling in Transition to Heart Failure With Normal Ejection Fraction
Heart failure with normal ejection fraction occurs in elderly patients with hypertensive heart disease. We hypothesized that, in such patients, mineralocorticoid receptor activation accelerates the types of ventricular and vascular remodeling and dysfunction believed important in the transition to h...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2008-02, Vol.51 (2), p.289-295 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Shapiro, Brian P Owan, Theophilus E Mohammed, Selma Kruger, Martina Linke, Wolfgang A Burnett, John C Redfield, Margaret M |
| description | Heart failure with normal ejection fraction occurs in elderly patients with hypertensive heart disease. We hypothesized that, in such patients, mineralocorticoid receptor activation accelerates the types of ventricular and vascular remodeling and dysfunction believed important in the transition to heart failure. We tested this hypothesis by administering deoxycorticosterone acetate (DOCA) without salt loading or nephrectomy to elderly dogs with experimental hypertension. Elderly dogs were made hypertensive by renal wrapping. After 5 weeks, dogs were randomly assigned to DOCA (1 mg/kg per day IM; old hypertensive [OH]+DOCA; n=11) or not (OH; n=11) for 3 weeks. At week 8, conscious echocardiography and hemodynamic assessment under anesthesia were performed. DOCA resulted in further increases in conscious blood pressure (P |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.107.099010 |
| format | Article |
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We hypothesized that, in such patients, mineralocorticoid receptor activation accelerates the types of ventricular and vascular remodeling and dysfunction believed important in the transition to heart failure. We tested this hypothesis by administering deoxycorticosterone acetate (DOCA) without salt loading or nephrectomy to elderly dogs with experimental hypertension. Elderly dogs were made hypertensive by renal wrapping. After 5 weeks, dogs were randomly assigned to DOCA (1 mg/kg per day IM; old hypertensive [OH]+DOCA; n=11) or not (OH; n=11) for 3 weeks. At week 8, conscious echocardiography and hemodynamic assessment under anesthesia were performed. DOCA resulted in further increases in conscious blood pressure (P<0.05) without increases in cardiac output or diastolic volume. In the conscious state, effective arterial elastance (P<0.05) and systemic vascular resistance (P=0.06) were increased, and systemic arterial compliance (P<0.05) was decreased in OH+DOCA animals. After anesthesia, instrumentation, and autonomic blockade, blood pressure was lower, whereas left ventricular (LV) systolic elastance, LV diastolic stiffness, and ex vivo myofiber diastolic stiffness were increased in OH+DOCA animals. LV collagen was increased in OH+DOCA animals (P<0.05 for all), but LV mass, LV brain natriuretic peptide, and titin isoform profiles were not. Neither aortic stiffness nor aortic structure was altered in OH+DOCA animals. These findings suggest that age and hypertensive heart disease enhance sensitivity to exogenous mineralocorticoid administration and that mineralocorticoid receptor activation could contribute to the transition to heart failure in elderly persons by promoting increases in LV diastolic and systolic stiffness.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.107.099010</identifier><identifier>PMID: 18086943</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Aging ; Animals ; Aorta - pathology ; Aorta - physiopathology ; Arterial hypertension. Arterial hypotension ; Arteries - physiopathology ; Biological and medical sciences ; Biomarkers - metabolism ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Cardiology. Vascular system ; Cardiotonic agents ; Cardiovascular system ; Collagen - metabolism ; Desoxycorticosterone - pharmacology ; Diastole ; Disease Models, Animal ; Disease Susceptibility ; Dogs ; Echocardiography ; Elasticity ; Heart Failure - etiology ; Heart Failure - physiopathology ; Heart Ventricles ; Hypertension - complications ; Hypertension - diagnostic imaging ; Hypertension - etiology ; Hypertension - physiopathology ; Hypertrophy, Left Ventricular - diagnostic imaging ; Medical sciences ; Mineralocorticoids - metabolism ; Myocardium - metabolism ; Pharmacology. Drug treatments ; Signal Transduction ; Stroke Volume ; Systole ; Vascular Resistance ; Vasomotor System - drug effects ; Vasomotor System - physiopathology ; Ventricular Function, Left</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2008-02, Vol.51 (2), p.289-295</ispartof><rights>2008 American Heart Association, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4852-1feb1c01ea32159caeb8e2b74b41a748bac6d841b9eff3555ef08ef56fe40df43</citedby><cites>FETCH-LOGICAL-c4852-1feb1c01ea32159caeb8e2b74b41a748bac6d841b9eff3555ef08ef56fe40df43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20032177$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18086943$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shapiro, Brian P</creatorcontrib><creatorcontrib>Owan, Theophilus E</creatorcontrib><creatorcontrib>Mohammed, Selma</creatorcontrib><creatorcontrib>Kruger, Martina</creatorcontrib><creatorcontrib>Linke, Wolfgang A</creatorcontrib><creatorcontrib>Burnett, John C</creatorcontrib><creatorcontrib>Redfield, Margaret M</creatorcontrib><title>Mineralocorticoid Signaling in Transition to Heart Failure With Normal Ejection Fraction</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Heart failure with normal ejection fraction occurs in elderly patients with hypertensive heart disease. We hypothesized that, in such patients, mineralocorticoid receptor activation accelerates the types of ventricular and vascular remodeling and dysfunction believed important in the transition to heart failure. We tested this hypothesis by administering deoxycorticosterone acetate (DOCA) without salt loading or nephrectomy to elderly dogs with experimental hypertension. Elderly dogs were made hypertensive by renal wrapping. After 5 weeks, dogs were randomly assigned to DOCA (1 mg/kg per day IM; old hypertensive [OH]+DOCA; n=11) or not (OH; n=11) for 3 weeks. At week 8, conscious echocardiography and hemodynamic assessment under anesthesia were performed. DOCA resulted in further increases in conscious blood pressure (P<0.05) without increases in cardiac output or diastolic volume. In the conscious state, effective arterial elastance (P<0.05) and systemic vascular resistance (P=0.06) were increased, and systemic arterial compliance (P<0.05) was decreased in OH+DOCA animals. After anesthesia, instrumentation, and autonomic blockade, blood pressure was lower, whereas left ventricular (LV) systolic elastance, LV diastolic stiffness, and ex vivo myofiber diastolic stiffness were increased in OH+DOCA animals. LV collagen was increased in OH+DOCA animals (P<0.05 for all), but LV mass, LV brain natriuretic peptide, and titin isoform profiles were not. Neither aortic stiffness nor aortic structure was altered in OH+DOCA animals. These findings suggest that age and hypertensive heart disease enhance sensitivity to exogenous mineralocorticoid administration and that mineralocorticoid receptor activation could contribute to the transition to heart failure in elderly persons by promoting increases in LV diastolic and systolic stiffness.</description><subject>Aging</subject><subject>Animals</subject><subject>Aorta - pathology</subject><subject>Aorta - physiopathology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Arteries - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - metabolism</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Cardiotonic agents</subject><subject>Cardiovascular system</subject><subject>Collagen - metabolism</subject><subject>Desoxycorticosterone - pharmacology</subject><subject>Diastole</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility</subject><subject>Dogs</subject><subject>Echocardiography</subject><subject>Elasticity</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Ventricles</subject><subject>Hypertension - complications</subject><subject>Hypertension - diagnostic imaging</subject><subject>Hypertension - etiology</subject><subject>Hypertension - physiopathology</subject><subject>Hypertrophy, Left Ventricular - diagnostic imaging</subject><subject>Medical sciences</subject><subject>Mineralocorticoids - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Signal Transduction</subject><subject>Stroke Volume</subject><subject>Systole</subject><subject>Vascular Resistance</subject><subject>Vasomotor System - drug effects</subject><subject>Vasomotor System - physiopathology</subject><subject>Ventricular Function, Left</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkG1r2zAQgMVYWbNuf2GYwfbN6Z0t-WXfQkmWQpeONWPdJyErp0adYnWSTem_r9aEFXpwp0M8d0IPYx8RpogVni5_f5__WM9XV-eXq9lyNkWop9C2gPCKTVAUPOeiKl-zCWDL8xbx-pi9jfEWADnn9Rt2jA00VcvLCbv-ZnsKynntw2C1t5vsyt70ytn-JrN9tg6qj3awvs8Gny1JhSFbKOvGQNkvO2yzlQ875bL5LeknahHUU_OOHRnlIr0_nCfs52K-PlvmF5dfz89mF7nmjShyNNShBiRVFiharahrqOhq3nFUNW86patNw7FryZhSCEEGGjKiMsRhY3h5wj7v994F_3ekOMidjZqcUz35McoairKFUiTwyx7UwccYyMi7YHcqPEgE-c-rfOE13ddy7zUNfzi8MnY72jyPHkQm4NMBUFErZ5I2beN_rgBI_6vrxPE9d-_dQCH-ceM9Bbkl5YathBS8qJo88Q2kAnnKoigfASREk9E</recordid><startdate>200802</startdate><enddate>200802</enddate><creator>Shapiro, Brian P</creator><creator>Owan, Theophilus E</creator><creator>Mohammed, Selma</creator><creator>Kruger, Martina</creator><creator>Linke, Wolfgang A</creator><creator>Burnett, John C</creator><creator>Redfield, Margaret M</creator><general>American Heart Association, Inc</general><general>Lippincott</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>200802</creationdate><title>Mineralocorticoid Signaling in Transition to Heart Failure With Normal Ejection Fraction</title><author>Shapiro, Brian P ; Owan, Theophilus E ; Mohammed, Selma ; Kruger, Martina ; Linke, Wolfgang A ; Burnett, John C ; Redfield, Margaret M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4852-1feb1c01ea32159caeb8e2b74b41a748bac6d841b9eff3555ef08ef56fe40df43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Aging</topic><topic>Animals</topic><topic>Aorta - pathology</topic><topic>Aorta - physiopathology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Arteries - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - metabolism</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Cardiotonic agents</topic><topic>Cardiovascular system</topic><topic>Collagen - metabolism</topic><topic>Desoxycorticosterone - pharmacology</topic><topic>Diastole</topic><topic>Disease Models, Animal</topic><topic>Disease Susceptibility</topic><topic>Dogs</topic><topic>Echocardiography</topic><topic>Elasticity</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Ventricles</topic><topic>Hypertension - complications</topic><topic>Hypertension - diagnostic imaging</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>Hypertrophy, Left Ventricular - diagnostic imaging</topic><topic>Medical sciences</topic><topic>Mineralocorticoids - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Signal Transduction</topic><topic>Stroke Volume</topic><topic>Systole</topic><topic>Vascular Resistance</topic><topic>Vasomotor System - drug effects</topic><topic>Vasomotor System - physiopathology</topic><topic>Ventricular Function, Left</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shapiro, Brian P</creatorcontrib><creatorcontrib>Owan, Theophilus E</creatorcontrib><creatorcontrib>Mohammed, Selma</creatorcontrib><creatorcontrib>Kruger, Martina</creatorcontrib><creatorcontrib>Linke, Wolfgang A</creatorcontrib><creatorcontrib>Burnett, John C</creatorcontrib><creatorcontrib>Redfield, Margaret M</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>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shapiro, Brian P</au><au>Owan, Theophilus E</au><au>Mohammed, Selma</au><au>Kruger, Martina</au><au>Linke, Wolfgang A</au><au>Burnett, John C</au><au>Redfield, Margaret M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mineralocorticoid Signaling in Transition to Heart Failure With Normal Ejection Fraction</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2008-02</date><risdate>2008</risdate><volume>51</volume><issue>2</issue><spage>289</spage><epage>295</epage><pages>289-295</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Heart failure with normal ejection fraction occurs in elderly patients with hypertensive heart disease. We hypothesized that, in such patients, mineralocorticoid receptor activation accelerates the types of ventricular and vascular remodeling and dysfunction believed important in the transition to heart failure. We tested this hypothesis by administering deoxycorticosterone acetate (DOCA) without salt loading or nephrectomy to elderly dogs with experimental hypertension. Elderly dogs were made hypertensive by renal wrapping. After 5 weeks, dogs were randomly assigned to DOCA (1 mg/kg per day IM; old hypertensive [OH]+DOCA; n=11) or not (OH; n=11) for 3 weeks. At week 8, conscious echocardiography and hemodynamic assessment under anesthesia were performed. DOCA resulted in further increases in conscious blood pressure (P<0.05) without increases in cardiac output or diastolic volume. In the conscious state, effective arterial elastance (P<0.05) and systemic vascular resistance (P=0.06) were increased, and systemic arterial compliance (P<0.05) was decreased in OH+DOCA animals. After anesthesia, instrumentation, and autonomic blockade, blood pressure was lower, whereas left ventricular (LV) systolic elastance, LV diastolic stiffness, and ex vivo myofiber diastolic stiffness were increased in OH+DOCA animals. LV collagen was increased in OH+DOCA animals (P<0.05 for all), but LV mass, LV brain natriuretic peptide, and titin isoform profiles were not. Neither aortic stiffness nor aortic structure was altered in OH+DOCA animals. These findings suggest that age and hypertensive heart disease enhance sensitivity to exogenous mineralocorticoid administration and that mineralocorticoid receptor activation could contribute to the transition to heart failure in elderly persons by promoting increases in LV diastolic and systolic stiffness.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>18086943</pmid><doi>10.1161/HYPERTENSIONAHA.107.099010</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 2008-02, Vol.51 (2), p.289-295 |
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| subjects | Aging Animals Aorta - pathology Aorta - physiopathology Arterial hypertension. Arterial hypotension Arteries - physiopathology Biological and medical sciences Biomarkers - metabolism Blood and lymphatic vessels Blood Pressure - drug effects Cardiology. Vascular system Cardiotonic agents Cardiovascular system Collagen - metabolism Desoxycorticosterone - pharmacology Diastole Disease Models, Animal Disease Susceptibility Dogs Echocardiography Elasticity Heart Failure - etiology Heart Failure - physiopathology Heart Ventricles Hypertension - complications Hypertension - diagnostic imaging Hypertension - etiology Hypertension - physiopathology Hypertrophy, Left Ventricular - diagnostic imaging Medical sciences Mineralocorticoids - metabolism Myocardium - metabolism Pharmacology. Drug treatments Signal Transduction Stroke Volume Systole Vascular Resistance Vasomotor System - drug effects Vasomotor System - physiopathology Ventricular Function, Left |
| title | Mineralocorticoid Signaling in Transition to Heart Failure With Normal Ejection Fraction |
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