Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene

Publikationen: Beitrag in FachzeitschriftZeitschriftenaufsätzeForschungBegutachtung

Standard

Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene. / Zobel, Carsten; Zavidou-Saroti, Persephone; Bölck, Birgit; Brixius, Klara; Reuter, Hannes; Frank, Konrad; Diedrichs, Holger; Müller-Ehmsen, Jochen; Bloch, Wilhelm; Schwinger, Robert H G.

in: European journal of applied physiology, Jahrgang 99, Nr. 2, 01.01.2007, S. 121-132.

Publikationen: Beitrag in FachzeitschriftZeitschriftenaufsätzeForschungBegutachtung

Harvard

Zobel, C, Zavidou-Saroti, P, Bölck, B, Brixius, K, Reuter, H, Frank, K, Diedrichs, H, Müller-Ehmsen, J, Bloch, W & Schwinger, RHG 2007, 'Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene', European journal of applied physiology, Jg. 99, Nr. 2, S. 121-132. https://doi.org/10.1007/s00421-006-0323-5

APA

Zobel, C., Zavidou-Saroti, P., Bölck, B., Brixius, K., Reuter, H., Frank, K., Diedrichs, H., Müller-Ehmsen, J., Bloch, W., & Schwinger, R. H. G. (2007). Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene. European journal of applied physiology, 99(2), 121-132. https://doi.org/10.1007/s00421-006-0323-5

Vancouver

Bibtex

@article{b85ee9ee6da14cd58c69fc5e6d72cd93,
title = "Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene",
abstract = "The present study aimed to characterize cardiac hypertrophy induced by activation of the renin-angiotensin system in terms of functional alterations on the level of the contractile proteins, employing transgenic rats harboring the mouse renin gene (TGR(mREN2)27). Ca2+-dependent tension and myosin ATPase activity were measured in skinned fiber preparations obtained from TGR(mREN2)27 and from age-matched Sprague-Dawley rats (SPDR). Western blots for troponin I (TnI) and troponin T (TnT) were performed and the phosphorylation status of TnI were evaluated in myocardial preparations. TnT and myosin heavy chain (MHC) isoforms were analyzed by RT-PCR. The pCa/tension relationship was shifted to the right in TGR(mREN2)27 compared to SPDR as indicated by increased Ca2+-concentrations required for half maximal activation of tension (SPDR 5.80, 95% confidence limits 5.77-5.82 vs. TGR(mREN2)27 5.69, 95% confidence limits 5.67-5.72, pCa units), while maximal developed tension was unaltered. Even more pronounced was the shift in the relationship between pCa and myosin-ATPase (SPDR 6.01, 95% confidence limits 5.99-6.03 vs. TGR(mREN2)27 5.77, 95% confidence limits 5.73-5.79, pCa units). The maximal myosin-ATPase activity was reduced in TGR(mREN2)27 compared to SPDR, respectively (211.0 +/- 28.77 micromol ADP/s vs. 271.6 +/- 43.66 micromol ADP/s, P < 0.05). Tension cost (ATPase activity/tension) was significantly reduced in TGR(mREN2)27. The beta-MHC expression was significantly increased in TGR(mREN2)27. There was no isoform shift for TnT (protein and mRNA), as well as TnI, and no alteration of the phosphorylation of TnI in TGR(mREN2)27 compared to SPRD. The present study demonstrates that cardiac hypertrophy, induced by an activation of the renin-angiotensin system, leads to adapting alterations on the level of the contractile filaments, which reduce tension cost.",
keywords = "Animals, Animals, Genetically Modified, Blotting, Western, Calcium, Cardiomegaly, Disease Models, Animal, Isometric Contraction, Linear Models, Male, Mice, Models, Cardiovascular, Muscle Tonus, Myocardial Contraction, Myosin Heavy Chains, Myosins, Papillary Muscles, Phosphorylation, RNA, Messenger, Rats, Rats, Sprague-Dawley, Renin, Reverse Transcriptase Polymerase Chain Reaction, Troponin I, Troponin T",
author = "Carsten Zobel and Persephone Zavidou-Saroti and Birgit B{\"o}lck and Klara Brixius and Hannes Reuter and Konrad Frank and Holger Diedrichs and Jochen M{\"u}ller-Ehmsen and Wilhelm Bloch and Schwinger, {Robert H G}",
year = "2007",
month = jan,
day = "1",
doi = "10.1007/s00421-006-0323-5",
language = "English",
volume = "99",
pages = "121--132",
journal = "European journal of applied physiology",
issn = "1439-6319",
publisher = "Springer Verlag",
number = "2",

}

RIS

TY - JOUR

T1 - Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene

AU - Zobel, Carsten

AU - Zavidou-Saroti, Persephone

AU - Bölck, Birgit

AU - Brixius, Klara

AU - Reuter, Hannes

AU - Frank, Konrad

AU - Diedrichs, Holger

AU - Müller-Ehmsen, Jochen

AU - Bloch, Wilhelm

AU - Schwinger, Robert H G

PY - 2007/1/1

Y1 - 2007/1/1

N2 - The present study aimed to characterize cardiac hypertrophy induced by activation of the renin-angiotensin system in terms of functional alterations on the level of the contractile proteins, employing transgenic rats harboring the mouse renin gene (TGR(mREN2)27). Ca2+-dependent tension and myosin ATPase activity were measured in skinned fiber preparations obtained from TGR(mREN2)27 and from age-matched Sprague-Dawley rats (SPDR). Western blots for troponin I (TnI) and troponin T (TnT) were performed and the phosphorylation status of TnI were evaluated in myocardial preparations. TnT and myosin heavy chain (MHC) isoforms were analyzed by RT-PCR. The pCa/tension relationship was shifted to the right in TGR(mREN2)27 compared to SPDR as indicated by increased Ca2+-concentrations required for half maximal activation of tension (SPDR 5.80, 95% confidence limits 5.77-5.82 vs. TGR(mREN2)27 5.69, 95% confidence limits 5.67-5.72, pCa units), while maximal developed tension was unaltered. Even more pronounced was the shift in the relationship between pCa and myosin-ATPase (SPDR 6.01, 95% confidence limits 5.99-6.03 vs. TGR(mREN2)27 5.77, 95% confidence limits 5.73-5.79, pCa units). The maximal myosin-ATPase activity was reduced in TGR(mREN2)27 compared to SPDR, respectively (211.0 +/- 28.77 micromol ADP/s vs. 271.6 +/- 43.66 micromol ADP/s, P < 0.05). Tension cost (ATPase activity/tension) was significantly reduced in TGR(mREN2)27. The beta-MHC expression was significantly increased in TGR(mREN2)27. There was no isoform shift for TnT (protein and mRNA), as well as TnI, and no alteration of the phosphorylation of TnI in TGR(mREN2)27 compared to SPRD. The present study demonstrates that cardiac hypertrophy, induced by an activation of the renin-angiotensin system, leads to adapting alterations on the level of the contractile filaments, which reduce tension cost.

AB - The present study aimed to characterize cardiac hypertrophy induced by activation of the renin-angiotensin system in terms of functional alterations on the level of the contractile proteins, employing transgenic rats harboring the mouse renin gene (TGR(mREN2)27). Ca2+-dependent tension and myosin ATPase activity were measured in skinned fiber preparations obtained from TGR(mREN2)27 and from age-matched Sprague-Dawley rats (SPDR). Western blots for troponin I (TnI) and troponin T (TnT) were performed and the phosphorylation status of TnI were evaluated in myocardial preparations. TnT and myosin heavy chain (MHC) isoforms were analyzed by RT-PCR. The pCa/tension relationship was shifted to the right in TGR(mREN2)27 compared to SPDR as indicated by increased Ca2+-concentrations required for half maximal activation of tension (SPDR 5.80, 95% confidence limits 5.77-5.82 vs. TGR(mREN2)27 5.69, 95% confidence limits 5.67-5.72, pCa units), while maximal developed tension was unaltered. Even more pronounced was the shift in the relationship between pCa and myosin-ATPase (SPDR 6.01, 95% confidence limits 5.99-6.03 vs. TGR(mREN2)27 5.77, 95% confidence limits 5.73-5.79, pCa units). The maximal myosin-ATPase activity was reduced in TGR(mREN2)27 compared to SPDR, respectively (211.0 +/- 28.77 micromol ADP/s vs. 271.6 +/- 43.66 micromol ADP/s, P < 0.05). Tension cost (ATPase activity/tension) was significantly reduced in TGR(mREN2)27. The beta-MHC expression was significantly increased in TGR(mREN2)27. There was no isoform shift for TnT (protein and mRNA), as well as TnI, and no alteration of the phosphorylation of TnI in TGR(mREN2)27 compared to SPRD. The present study demonstrates that cardiac hypertrophy, induced by an activation of the renin-angiotensin system, leads to adapting alterations on the level of the contractile filaments, which reduce tension cost.

KW - Animals

KW - Animals, Genetically Modified

KW - Blotting, Western

KW - Calcium

KW - Cardiomegaly

KW - Disease Models, Animal

KW - Isometric Contraction

KW - Linear Models

KW - Male

KW - Mice

KW - Models, Cardiovascular

KW - Muscle Tonus

KW - Myocardial Contraction

KW - Myosin Heavy Chains

KW - Myosins

KW - Papillary Muscles

KW - Phosphorylation

KW - RNA, Messenger

KW - Rats

KW - Rats, Sprague-Dawley

KW - Renin

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Troponin I

KW - Troponin T

U2 - 10.1007/s00421-006-0323-5

DO - 10.1007/s00421-006-0323-5

M3 - Journal articles

C2 - 17063360

VL - 99

SP - 121

EP - 132

JO - European journal of applied physiology

JF - European journal of applied physiology

SN - 1439-6319

IS - 2

ER -

ID: 70429