Role of renin-angiotensin system in development of heart failure induced by myocardial infarction in rats

Trindade, Daniel C.; Trindade, Raquel C.; Marassi, Michelle P.; Martins, Ornélia P.P.R.; Costa-e-Sousa, Ricardo H.; Mattos, Elisabete C.; Jr., A. Marinho; Reis, L. C.; Olivares, Emerson Lopes

doi:10.1590/s0001-37652007000200008

Cited by 8 publications

(17 citation statements)

References 18 publications

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“…Experiments in animal and human have been indicated that the activation of the renin-angiotensin system plays a crucial role in the progression of MI [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…Angiotensin-(1-7) [ANG- (1)(2)(3)(4)(5)(6)(7)] is an endogenous peptide of the renin-angiotensin system. It has been suggested that the cardiovascular system is the main target for the ANG-(1-7) actions.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, an extensive body of scientific work supports the protective effects of ANG-(1-7) on the cardiovascular system through its interactions with the specific receptor Mas [8,9]. [D-Ala7]-Ang-(1-7) (A-779) is a potent and selective ANG- (1)(2)(3)(4)(5)(6)(7) antagonist. This compound antagonizes several actions of ANG-(1-7) [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

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Impairment of Cardiac Function and Remodeling Induced by Myocardial Infarction in Rats are Attenuated by the Nonpeptide Angiotensin‐(1–7) Analog AVE 0991

Zeng

Chen

Leng

et al. 2010

Cardiovascular Therapeutics

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SUMMARY Aims:We evaluated effects of the nonpeptide angiotensin (ANG)-(1-7) analog AVE 0991 (AVE) on cardiac function and remodeling as well as transforming growth factor-beta1 (TGF-β1)/tumor necrosis factor-alpha (TNF-α) expression in myocardial infarction rat models. Methods and Results: Sprague-Dawley rats underwent either sham surgery or coronary ligation. They were divided into four groups: sham, control, AVE, and AVE+A-779 ]-ANG-(1-7), a selective antagonist for the ANG-(1-7)] group. After 4 weeks of treatment, the AVE group displayed a significant elevation in left ventricular fractional shorting (LVFS) (25.5 ± 7.3% vs. 18.4 ± 3.3%, P < 0.05) and left ventricular ejection fraction (LVEF) (44.8 ± 7.6% vs. 32.7 ± 6.5%, P < 0.05) when compared to the control group, but no effects on the left ventricular end-diastolic and end-systolic diameters (LVDd and LVDs, respectively) were observed. In addition, we found that the myocyte diameter (18 ± 2 μm vs. 22 ± 4 μm, P < 0.05), infarct size (42.6 ± 3.6% vs. 50.9 ± 4.4%, P < 0.001) and collagen volume fraction (CVF) (16.4 ± 2.2% vs. 25.3 ± 3.2%, P < 0.001) were significantly reduced in the AVE group when compared to the control group. There were no differences in LVFS, LVEF, myocyte diameter, and infarct size between the control and AVE+A-779 groups. AVE also markedly attenuated the increased mRNA expression of collagen I (P < 0.001) and collagen III (P < 0.001) and inhibited the overexpression of TGF-β1 (P < 0.05) and TNF-α (P < 0.05) compared to the control group. Conclusion: AVE could improve cardiac function and attenuate ventricular remodeling in MI rat models. It may involve the inhibition of inflammatory factors TGF-β1/TNF-α overexpression and the action on the specific receptor Mas of ANG-(1-7).

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“…Experiments in animal and human have been indicated that the activation of the renin-angiotensin system plays a crucial role in the progression of MI [3,4].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impairment of Cardiac Function and Remodeling Induced by Myocardial Infarction in Rats are Attenuated by the Nonpeptide Angiotensin‐(1–7) Analog AVE 0991

Zeng

Chen

Leng

et al. 2010

Cardiovascular Therapeutics

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“…LV dilatation was reduced, and the deterioration of LV function and LV remodeling were attenuated by treatment with either captopril or amlodipine; however, control levels were not achieved. [27][28][29][30] The Systolic Hypertension in Europe (Syst-Eur) study demonstrated that a delay in therapy onset was associated with a significantly higher occurrence of cardiovascular complications. 31 This finding is in full agreement with our echocardiography and heart catheterization results, which clearly show that antihypertensive treatment with either a CAP monotherapy or a combination of CAP and NIF delayed cardiac hypertrophy and the deterioration of LV function in SRHs but could not completely prevent them.…”

Section: Discussionmentioning

confidence: 99%

Effects of late-onset and long-term captopril and nifedipine treatment in aged spontaneously hypertensive rats: Echocardiographic studies

Zimmer

Hawlitschek

Rabald³

et al. 2015

Hypertens Res

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The purpose of the present study was to analyze the changes in blood pressure, left ventricular (LV) wall thickness and LV systolic function of aged spontaneously hypertensive rats (SHRs) either with or without antihypertensive therapy. Twenty-one SHRs aged 60.5±0.25 weeks were investigated over 22 weeks. They were divided into the following three groups (7 per group): untreated controls (CTRL), treatment with captopril (CAP, 60 mg kg(-1) daily) and treatment with captopril plus nifedipine (CAP+NIF, 60+10 mg kg(-1) daily). Systolic blood pressure (SBP) was regularly measured using the tail cuff method, and an echocardiogram was repeatedly obtained to examine the LV systolic and diastolic area, LV systolic fractional area change, cardiac output and LV myocardial wall thickness. Finally, heart catheterization was performed. While SBP remained stable in the CTRL animals over the experimental period, both of the antihypertensive treatments significantly reduced SBP by 20% in the treated animals (P<0.001). Echocardiography demonstrated that both the systolic and the diastolic LV function of the untreated SHRs deteriorated over time, whereas both types of antihypertensive treatments attenuated and delayed but did not completely prevent the decline in LV systolic function. Cardiac output, as determined by pulsed wave Doppler echocardiography, remained significantly higher in the treated animals than in CTRLs until week 20, but it then decreased. Heart catheterization showed a significant decrease in LV function, as reflected by the LV systolic pressure and contractility, in the CTRLs but not in treated animals. These findings clearly indicate that late-onset antihypertensive treatment with CAP or CAP+NIF is beneficial with respect to blood pressure reduction, LV hypertrophy attenuation and LV systolic function preservation.

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“…Experimental data support its effectiveness in blocking CHF‐induced neuroendocrine activation and improving cardiac performance 3,4 . Beneficial effects have also been demonstrated by our group 5 . Trindade et al .…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Brain Renin–angiotensin System Improves Diastolic Cardiac Function Following Myocardial Infarction in Rats

Araujo¹,

Trindade²,

Mecawi³

et al. 2009

Clin Exp Pharma Physio

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1. Recently, we demonstrated that oral captopril treatment improved diastolic function and attenuated cardiac remodelling after myocardial infarction (MI) in rats. Considering the feasible role of the brain renin-angiotensin system (RAS) in heart failure, in the present study we investigated the role of the captopril injected intracerebroventricularly (i.c.v.) on the progression of cardiac dysfunction. 2. Male Wistar rats underwent experimental MI or sham operation. Infarcted animals received daily i.c.v. injections of captopril (approximately 200 mg/kg; MI + Cap) or saline (MI) from 11 to 18 days after infarction. Electro- and echocardiogram assessments were performed before and after i.c.v. treatment (10 and 18 days after MI, respectively). Water and hypertonic saline ingestion were determined daily between 12 and 16 days after MI. 3. Electrocardiograms from the MI and MI + Cap groups showed signs that resembled large MI before and after i.c.v. treatment. However, despite similar systolic dysfunction observed in both groups, only captopril-treated rats exhibited reduced left ventricular (LV) dilatation and improved LV filling, as assessed by echocardiograms, and low levels of water ingestion compared with the saline-treated control group. 4. The results of the present study suggest that the brain RAS may participate in the development of cardiac dysfunction induced by ischaemia and that inhibition of the brain RAS may provide a new strategy for the prevention of diastolic dysfunction.

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Role of renin-angiotensin system in development of heart failure induced by myocardial infarction in rats

Cited by 8 publications

References 18 publications

Impairment of Cardiac Function and Remodeling Induced by Myocardial Infarction in Rats are Attenuated by the Nonpeptide Angiotensin‐(1–7) Analog AVE 0991

Impairment of Cardiac Function and Remodeling Induced by Myocardial Infarction in Rats are Attenuated by the Nonpeptide Angiotensin‐(1–7) Analog AVE 0991

Effects of late-onset and long-term captopril and nifedipine treatment in aged spontaneously hypertensive rats: Echocardiographic studies

Inhibition of Brain Renin–angiotensin System Improves Diastolic Cardiac Function Following Myocardial Infarction in Rats

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