PortalPublikationenActivation of the cardiac endothelin system in left ventricu...

Activation of the cardiac endothelin system in left ventricular hypertrophy before onset of heart failure in TG(mREN2)27 rats.

Standard

Activation of the cardiac endothelin system in left ventricular hypertrophy before onset of heart failure in TG(mREN2)27 rats. / Zolk, Oliver; Quattek, Jessika; Seeland, Ute; El-Armouche, Ali; Eschenhagen, Thomas; Böhm, Michael.

in: CARDIOVASC RES, Jahrgang 53, Nr. 2, 2, 2002, S. 363-371.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Zolk, O, Quattek, J, Seeland, U, El-Armouche, A, Eschenhagen, T & Böhm, M 2002, 'Activation of the cardiac endothelin system in left ventricular hypertrophy before onset of heart failure in TG(mREN2)27 rats.', CARDIOVASC RES, Jg. 53, Nr. 2, 2, S. 363-371. <http://www.ncbi.nlm.nih.gov/pubmed/11827687?dopt=Citation>

APA

Zolk, O., Quattek, J., Seeland, U., El-Armouche, A., Eschenhagen, T., & Böhm, M. (2002). Activation of the cardiac endothelin system in left ventricular hypertrophy before onset of heart failure in TG(mREN2)27 rats. CARDIOVASC RES, 53(2), 363-371. [2]. http://www.ncbi.nlm.nih.gov/pubmed/11827687?dopt=Citation

Vancouver

Zolk O, Quattek J, Seeland U, El-Armouche A, Eschenhagen T, Böhm M. Activation of the cardiac endothelin system in left ventricular hypertrophy before onset of heart failure in TG(mREN2)27 rats. CARDIOVASC RES. 2002;53(2):363-371. 2.

Bibtex

@article{46b8030bf76f4b609e7d226e0009066c,
title = "Activation of the cardiac endothelin system in left ventricular hypertrophy before onset of heart failure in TG(mREN2)27 rats.",
abstract = "OBJECTIVE: To characterize the cardiac angiotensin and endothelin (ET) system in compensated left ventricular hypertrophy due to long standing arterial hypertension and to assess the role of angiotensin and ET converting enzymes in mediating the observed changes of angiotensin and ET levels, respectively. METHODS: We studied the left ventricular renin-angiotensin system (RAS) and ET system in 20-week-old male transgenic hypertensive TG(mREN2)27 rats, a model of the monogenic renin-dependent form of severe hypertension. Age-matched Sprague-Dawley rats served as controls. RESULTS: TG(mREN2)27 rats exhibited left ventricular hypertrophy without signs of congestion. Transgene overexpression led to an activation of the tissue RAS with increased angiotensin II levels in spite of unchanged angiotensin converting enzyme (ACE) activity and ACE mRNA levels. ET-1 production was markedly increased in TG(mREN2)27 rats indicating that the ET-system was activated. Cardiac ET-1 in TG(mREN2)27 originated most likely from increased preproET-1 production because preproET-1 mRNA levels were increased but ET converting enzyme gene expression and activity were unchanged. Furthermore, ET-1 binding sites were significantly increased in TG(mREN2)27 rats without changes in K(D) values and ET(A)/ET(B) receptor ratios. ET(A) receptor gene expression was not altered whereas ET(B) receptor mRNA levels were up-regulated twofold in TG(mREN2)27 rats suggesting that ET(A) and ET(B) receptor expression may be regulated differentially. CONCLUSIONS: Cardiac ET and angiotensin systems are co-activated in compensated cardiac hypertrophy before onset of heart failure, and thus may be involved in the mechanism by which cardiac remodelling and progression of left ventricular dysfunction occur in TG(mREN2)27 rats.",
author = "Oliver Zolk and Jessika Quattek and Ute Seeland and Ali El-Armouche and Thomas Eschenhagen and Michael B{\"o}hm",
year = "2002",
language = "Deutsch",
volume = "53",
pages = "363--371",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Activation of the cardiac endothelin system in left ventricular hypertrophy before onset of heart failure in TG(mREN2)27 rats.

AU - Zolk, Oliver

AU - Quattek, Jessika

AU - Seeland, Ute

AU - El-Armouche, Ali

AU - Eschenhagen, Thomas

AU - Böhm, Michael

PY - 2002

Y1 - 2002

N2 - OBJECTIVE: To characterize the cardiac angiotensin and endothelin (ET) system in compensated left ventricular hypertrophy due to long standing arterial hypertension and to assess the role of angiotensin and ET converting enzymes in mediating the observed changes of angiotensin and ET levels, respectively. METHODS: We studied the left ventricular renin-angiotensin system (RAS) and ET system in 20-week-old male transgenic hypertensive TG(mREN2)27 rats, a model of the monogenic renin-dependent form of severe hypertension. Age-matched Sprague-Dawley rats served as controls. RESULTS: TG(mREN2)27 rats exhibited left ventricular hypertrophy without signs of congestion. Transgene overexpression led to an activation of the tissue RAS with increased angiotensin II levels in spite of unchanged angiotensin converting enzyme (ACE) activity and ACE mRNA levels. ET-1 production was markedly increased in TG(mREN2)27 rats indicating that the ET-system was activated. Cardiac ET-1 in TG(mREN2)27 originated most likely from increased preproET-1 production because preproET-1 mRNA levels were increased but ET converting enzyme gene expression and activity were unchanged. Furthermore, ET-1 binding sites were significantly increased in TG(mREN2)27 rats without changes in K(D) values and ET(A)/ET(B) receptor ratios. ET(A) receptor gene expression was not altered whereas ET(B) receptor mRNA levels were up-regulated twofold in TG(mREN2)27 rats suggesting that ET(A) and ET(B) receptor expression may be regulated differentially. CONCLUSIONS: Cardiac ET and angiotensin systems are co-activated in compensated cardiac hypertrophy before onset of heart failure, and thus may be involved in the mechanism by which cardiac remodelling and progression of left ventricular dysfunction occur in TG(mREN2)27 rats.

AB - OBJECTIVE: To characterize the cardiac angiotensin and endothelin (ET) system in compensated left ventricular hypertrophy due to long standing arterial hypertension and to assess the role of angiotensin and ET converting enzymes in mediating the observed changes of angiotensin and ET levels, respectively. METHODS: We studied the left ventricular renin-angiotensin system (RAS) and ET system in 20-week-old male transgenic hypertensive TG(mREN2)27 rats, a model of the monogenic renin-dependent form of severe hypertension. Age-matched Sprague-Dawley rats served as controls. RESULTS: TG(mREN2)27 rats exhibited left ventricular hypertrophy without signs of congestion. Transgene overexpression led to an activation of the tissue RAS with increased angiotensin II levels in spite of unchanged angiotensin converting enzyme (ACE) activity and ACE mRNA levels. ET-1 production was markedly increased in TG(mREN2)27 rats indicating that the ET-system was activated. Cardiac ET-1 in TG(mREN2)27 originated most likely from increased preproET-1 production because preproET-1 mRNA levels were increased but ET converting enzyme gene expression and activity were unchanged. Furthermore, ET-1 binding sites were significantly increased in TG(mREN2)27 rats without changes in K(D) values and ET(A)/ET(B) receptor ratios. ET(A) receptor gene expression was not altered whereas ET(B) receptor mRNA levels were up-regulated twofold in TG(mREN2)27 rats suggesting that ET(A) and ET(B) receptor expression may be regulated differentially. CONCLUSIONS: Cardiac ET and angiotensin systems are co-activated in compensated cardiac hypertrophy before onset of heart failure, and thus may be involved in the mechanism by which cardiac remodelling and progression of left ventricular dysfunction occur in TG(mREN2)27 rats.

M3 - SCORING: Zeitschriftenaufsatz

VL - 53

SP - 363

EP - 371

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 2

M1 - 2

ER -