Effect of captopril on the prevention and regression of myocardial cell hypertrophy and interstitial fibrosis in pressure overload cardiac hypertrophy

Rossi, Marcos A.; Peres, Luíz César

doi:10.1016/0002-8703(92)90281-y

Cited by 76 publications

(38 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The decrease in the heart weight elicited by captopril treatment in the sham-operated rats is consistent with earlier reports by Rossi et al 38 The results of the present study suggest the possibility that DGK⑀ is involved in the signal transduction of the renin-angiotensin system in cardiac myocytes in terms of regulating the normal growth of the LV.…”

Section: Dgk⑀ Gene Expression and The Effects Of Captoprilsupporting

confidence: 93%

Gene Expression and In Situ Localization of Diacylglycerol Kinase Isozymes in Normal and Infarcted Rat Hearts

Takeda

Kagaya

Takahashi

et al. 2001

Circulation Research

View full text Add to dashboard Cite

Abstract-Diacylglycerol (DG) kinase (DGK) terminates signaling from DG, which serves as an activator of protein kinase C (PKC), by converting DG to phosphatidic acid. DGK is thus regarded as an attenuator of the PKC activity. In rats, five DGK isozymes have been cloned, but little is known about their role in the heart. In this study, the spatiotemporal expression of DGK isozymes was investigated in rat hearts under a normal condition and after myocardial infarction (MI) by in situ hybridization histochemistry and immunohistochemistry. In normal left ventricular myocardium, DGK␣, DGK⑀, and DGK mRNAs were expressed evenly throughout the myocardium, although the DGK␣ expression was very low. In infarcted hearts, the expression of DGK was enhanced in the peripheral zone of the necrotic area and at the border zone 3 and 7 days after MI, and to a lesser extent in the middle layer of the granulation tissue 21 days after MI. The enhanced DGK expression in the infarcted and border areas could be attributed to granulocytes and macrophages. In contrast, the expression of DGK⑀ in the infarcted and border areas was lower than that in the viable left ventricle (LV) throughout the postoperation period. Furthermore, DGK⑀ expression in the viable myocardium 21 days after MI decreased significantly compared with left ventricular myocardium in the sham-operated rats and was completely restored by treatment with captopril. Our results demonstrate that three DGK isozymes are expressed in the heart and that each isozyme might have different functional characteristics in the healing and LV remodeling after MI.

show abstract

Section: Dgk⑀ Gene Expression and The Effects Of Captoprilsupporting

confidence: 93%

Gene Expression and In Situ Localization of Diacylglycerol Kinase Isozymes in Normal and Infarcted Rat Hearts

Takeda

Kagaya

Takahashi

et al. 2001

Circulation Research

View full text Add to dashboard Cite

show abstract

“…26 It remains unclear whether regression of epicardial vascular remodeling is accompanied by improvement in microcirculatory function in humans, 27 although it has been demonstrated in animal models. 28 The effect of intraventricular pressure changes on MBF is also poorly understood, with conflicting evidence from animal models. 29,30 In our study there was a clear relationship between a reduction in hemodynamic workload, as demonstrated by the change in AVA, and increase in CVR, which, in the absence of epicardial stenosis, suggests an improvement in coronary microcirculatory function in these patients after AVR.…”

Section: Changes In Coronary Perfusion and Microcirculatory Function mentioning

confidence: 99%

Functional Changes in Coronary Microcirculation After Valve Replacement in Patients With Aortic Stenosis

et al. 2003

View full text Add to dashboard Cite

Background-Increased extravascular compression and reduced diastolic perfusion time (DPT), rather than vascular remodeling, influence coronary microcirculatory dysfunction in aortic stenosis (AS). However, alterations after aortic valve replacement (AVR) remain unclear. The aim of the present study was to quantify changes in transmural perfusion and coronary vasodilator reserve (CVR), a measure of microcirculatory function, after AVR and determine the relative contribution of left ventricular mass (LVM) regression, change in aortic valve area (AVA), and DPT. Methods and Results-Twenty-two patients with AS were studied before and 1 year after AVR using echocardiography to measure AVA, cardiovascular magnetic resonance to assess LVM, and positron emission tomography to quantify resting and hyperemic myocardial blood flow (MBF) and CVR. Regression of LVM occurred in all patients (from 129Ϯ30 to 94Ϯ24 g/m 2 ; PϽ0.0001), and there was a significant reduction in resting MBF and increase in CVR corrected for rate-pressure product after AVR, although these changes displayed marked heterogeneity. Regression of LVM was linearly related to change in resting total LV blood flow but not CVR. Increase in hyperemic MBF and CVR transmurally was directly related to the increase in AVA after AVR. A significant relationship existed between the change in hyperemic DPT (1.0Ϯ4.7 s/min [range, 6.8 to 9.6]) and change in transmural CVR (yϭ0.08xϩ0.18; rϭ0.44; Pϭ0.04). Conclusions-Changes

show abstract

“…A variety of experimental models have been proposed to investigate pressure overload-induced CR [4][5][6] . More recently, Exercise tolerance and aortic stenosis Arq Bras Cardiol.…”

Section: Introductionmentioning

confidence: 99%

Tolerância ao esforço em ratos com estenose aórtica e disfunção ventricular diastólica e/ou sistólica

Mendes

Sugizaki

Campos

et al. 2013

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

show abstract

Effect of captopril on the prevention and regression of myocardial cell hypertrophy and interstitial fibrosis in pressure overload cardiac hypertrophy

Cited by 76 publications

References 46 publications

Gene Expression and In Situ Localization of Diacylglycerol Kinase Isozymes in Normal and Infarcted Rat Hearts

Gene Expression and In Situ Localization of Diacylglycerol Kinase Isozymes in Normal and Infarcted Rat Hearts

Functional Changes in Coronary Microcirculation After Valve Replacement in Patients With Aortic Stenosis

Tolerância ao esforço em ratos com estenose aórtica e disfunção ventricular diastólica e/ou sistólica

Contact Info

Product

Resources

About