Long-term Carperitide Treatment Attenuates Left Ventricular Remodeling in Rats With Heart Failure After Autoimmune Myocarditis

Tanaka, Komei; Ito, Masahiro; Kodama, Makoto; Hoyano, Makoto; Kimura, Satoshi; Mitsuma, Wataru; Hirono, Shuichi; Adachi, Takeshi; Watanabe, Kenichi; Nakazawa, Makoto; Aizawa, Yoshifusa

doi:10.1097/fjc.0b013e3181b0cf50

Cited by 5 publications

(2 citation statements)

References 31 publications

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“…Animal models of cardiovascular disease have shown the role of the natriuretic peptide system in precipitating myocardial disease states with progression to heart failure. Similarly, carperitide treatment for 4 weeks limited the extent of left ventricular remodeling in rats with autoimmune myocarditis [78]. BNP treatment for 3 weeks in dogs with chronic myocardial ischemia preserved left ventricular geometry, improved systolic function, and prevented the progression of systolic heart failure compared with control [76].…”

Section: Insights From Animal Models Of Heart Failurementioning

confidence: 96%

Natriuretic peptides in animal models of cardiovascular disease

Burley

Bice

Baxter

2014

Cardiovascular Endocrinology

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Natriuretic peptides play a major role in cardiovascular homeostasis, and much of our knowledge on this stems from animal studies looking into the genetic knockout or overexpression of natriuretic peptides or their biological target, the natriuretic peptide receptor. Genetic perturbation of the natriuretic peptide system in rodents causes systemic hypertension, cardiac fibrosis, left ventricular hypertrophy, and heart failure. Moreover, animal models of acute myocardial infarction and heart failure have demonstrated the therapeutic potential of exogenously administered natriuretic peptides in treating human acute coronary syndromes and heart failure. In this review, we hope to highlight the importance of animal models in helping us understand the biological function and consequence of the natriuretic peptide system in cardiovascular disease.

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Section: Insights From Animal Models Of Heart Failurementioning

confidence: 96%

Natriuretic peptides in animal models of cardiovascular disease

Burley

Bice

Baxter

2014

Cardiovascular Endocrinology

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“…[3][4][5][6] We have been interested in proteins that correlate well with the progression of EAM-induced heart failure. In the present study, we conducted a proteomic analysis to specify and identify proteins which correlate well with the changes in cardiac function in the chronic phase of heart failure.…”

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confidence: 99%

Functional Proteomic Analysis of Experimental Autoimmune Myocarditis-Induced Chronic Heart Failure in the Rat

Sanzen

Ito

Ohta

et al. 2010

Biological & Pharmaceutical Bulletin

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Congenital or acquired problems in myocardium cause heart failure. To study congenital heart failure, we have used TO-2 hamsters.1,2) To study the acquired type, we have used experimental autoimmune myocarditis (EAM). The immunization of Lewis rats with pig cardiac myosin results in acute myocarditis-induced heart failure followed around 8 weeks late by a stable chronic phase.3) We have investigated the therapeutic effects of several drugs and conducted etiological studies in the acute and chronic phases of heart failure using the EAM model. [3][4][5][6] We have been interested in proteins that correlate well with the progression of EAM-induced heart failure. In the present study, we conducted a proteomic analysis to specify and identify proteins which correlate well with the changes in cardiac function in the chronic phase of heart failure. Although there have been several reports of proteomic analyses of heart failure, 7-11) none was on EAM-induced heart failure. Moreover, these reports compared only levels of proteins with those in normal heart, and did not examine the correlation between protein expression and cardiac function. A detailed comparison of changes in protein expression with changes in the heart function of the failing heart would provide insights into the mechanisms underlying myocardial remodeling and deterioration and may lead to the discovery of potential drug targets.In this study, we performed a detailed comparison of changes in protein expression in the EAM-induced chronic heart failure model with heart function and pathological parameters. We focused on major proteins in myocardium prefractionated into membranous (M) and soluble (S) fractions.We found several proteins, including glucose regulated protein (GRP)78 and heat shock protein (HSP)90b which showed excellent correlations between their levels and heart functions. MATERIALS AND METHODS Animals and ProceduresNine-week-old male Lewis rats (Charles River Japan Inc., Kanagawa, Japan) were used. Autoimmune myocarditis was induced as described previously.3) Ten immunized rats were used as a heart failure group (HF-group) and 10 age-matched normal Lewis rats were used as a control group (N-group). The morbidity of experimental autoimmune myocarditis was 100%. The acute phase of myocarditis-induced heart failure ceased at around 4 weeks and stable chronic heart failure developed. The rats were used at 8 weeks after immunization (HF-group). The protocol was approved by the Committee on the Guidelines for Animal Experimentation of Niigata University. All animals were treated in accordance with the guidelines for animal experiments as laid out by our institute.Measurement of Hemodynamic Parameters Echo cardiographs and hemodynamic parameters were measured under 2% isoflurane in pure oxygen gas anesthesia with spontaneous respiration.1,3) B-and M-mode echo-cardiograms were obtained using a linear scan probe (13 MHz, EUB6500, Hitachi, Tokyo, Japan). The ejection fraction (EF) and fractional shortening (FS) were calculated. Left ventricular press...

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Atrial natriuretic peptide exerts protective action against angiotensin II-induced cardiac remodeling by attenuating inflammation via endothelin-1/endothelin receptor A cascade

et al. 2013

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We aimed to investigate whether atrial natriuretic peptide (ANP) attenuates angiotensin II (Ang II)-induced myocardial remodeling and to clarify the possible molecular mechanisms involved. Thirty-five 8-week-old male Wistar-Kyoto rats were divided into control, Ang II, Ang II + ANP, and ANP groups. The Ang II and Ang II + ANP rats received 1 μg/kg/min Ang II for 14 days. The Ang II + ANP and ANP rats also received 0.1 μg/kg/min ANP intravenously. The Ang II and Ang II + ANP rats showed comparable blood pressure. Left ventricular fractional shortening and ejection fraction were lower in the Ang II rats than in controls; these indices were higher (P < 0.001) in the Ang II + ANP rats than in the Ang II rats. In the Ang II rats, the peak velocity of mitral early inflow and its ratio to atrial contraction-related peak flow velocity were lower, and the deceleration time of mitral early inflow was significantly prolonged; these changes were decreased by ANP. Percent fibrosis was higher (P < 0.001) and average myocyte diameters greater (P < 0.01) in the Ang II rats than in controls. ANP decreased both myocardial fibrosis (P < 0.01) and myocyte hypertrophy (P < 0.01). Macrophage infiltration, expression of mRNA levels of collagen types I and III, monocyte chemotactic protein-1, and a profibrotic/proinflammatory molecule, tenascin-C (TN-C) were increased in the Ang II rats; ANP significantly decreased these changes. In vitro, Ang II increased expression of TN-C and endothelin-1 (ET-1) in cardiac fibroblasts, which were reduced by ANP. ET-1 upregulated TN-C expression via endothelin type A receptor. These results suggest that ANP may protect the heart from Ang II-induced remodeling by attenuating inflammation, at least partly through endothelin 1/endothelin receptor A cascade.

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Long-term Carperitide Treatment Attenuates Left Ventricular Remodeling in Rats With Heart Failure After Autoimmune Myocarditis

Cited by 5 publications

References 31 publications

Natriuretic peptides in animal models of cardiovascular disease

Natriuretic peptides in animal models of cardiovascular disease

Functional Proteomic Analysis of Experimental Autoimmune Myocarditis-Induced Chronic Heart Failure in the Rat

Atrial natriuretic peptide exerts protective action against angiotensin II-induced cardiac remodeling by attenuating inflammation via endothelin-1/endothelin receptor A cascade

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