Captopril Treatment Improves the Sarcoplasmic Reticular Ca2+Transport in Heart Failure Due to Myocardial Infarction

Shao, Qiming; Ren, Bin; Zarain‐Herzberg, Ángel; Ganguly, Pallab K.; Dhalla, Naranjan S.

doi:10.1006/jmcc.1999.1000

Cited by 35 publications

(32 citation statements)

References 30 publications

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“…Captopril attenuated the reduction in the SR Ca 2ϩ pump and phospholamban protein contents, and the mRNA levels for SERCA2 and phospholamban in the failing rat heart, because of myocardial infarction. 28 In the present study, enalapril significantly improved the changes in the expression of SERCA2; however, FR attenuated the effect of enalapril on the upregulation of the SERCA2 gene. Endogenous BK may exert a beneficial effect on the status of SR Ca 2ϩ transport in the failing heart and improve LV diastolic properties under long-term treatment of an ACEI.…”

Section: Discussioncontrasting

confidence: 56%

Bradykinin Improves Left Ventricular Diastolic Function Under Long-Term Angiotensin-Converting Enzyme Inhibition in Heart Failure

et al. 2002

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Abstract-Both systolic and diastolic cardiac dysfunction coexist in various degrees in the majority of patients with heart failure. Although ACE inhibitors are useful in the treatment of heart failure, the roles of bradykinin in the systolic and diastolic properties of left ventricular function under long-term treatment of ACE inhibitor have not been fully elucidated. We therefore evaluated the changes in left ventricular function, histomorphometry, and the expression of several failing heart related genes, by use of an orally active specific bradykinin type 2 receptor antagonist, FR173657 (0.3 mg/kg per day), with an ACE inhibitor, enalapril (1 mg/kg per day), in dogs with tachycardia-induced heart failure (270 ppm, 22 days) and compared the effects to enalapril alone. Although there were no differences observed in blood pressure, left ventricular dimension, and percentage of fractional shortening, FR173657 significantly increased left ventricular filling pressure (PϽ0.01), prolonged the time constant of relaxation (PϽ0.05), and suppressed the expression of endothelial NO synthase and sarcoplasmic reticulum Ca 2ϩ -ATPase mRNA (PϽ0.05). FR173657 also upregulated collagen type I and III mRNA (PϽ0.05) and increased the total amount of cardiac collagen deposits (PϽ0.05) in left ventricle compared with that in the enalapril-treated group. In conclusion, endogenous bradykinin contributes to the cardioprotective effect of ACE inhibitor, improving left ventricular diastolic dysfunction rather than systolic dysfunction, via modification of NO release and Ca 2ϩ handling and suppression of collagen accumulation. Key Words: angiotensin-converting enzyme Ⅲ bradykinin Ⅲ Ca 2ϩ -transponding ATPase Ⅲ diastole Ⅲ fibrosis Ⅲ heart failure Ⅲ ventricular function, left A ngiotensin-converting enzyme inhibitors (ACEIs) exert beneficial effects on cardiac contractile function and are useful in improving both the symptoms and survival rate of a broad spectrum of patients with congestive heart failure (CHF). 1 In addition to suppressing the formation of angiotensin (Ang) II, the agents also prevent the breakdown of the potent vasodilator bradykinin (BK), which exerts its vasodilative action through BK type 2 (B 2 ) receptors. 2 Cardiomyocytes and cardiac fibroblasts have the capacity to generate BK, and they express functional B 2 receptors. BK possesses not only vasodilative action but also inotropic and antiproliferative properties. 3 Indeed, an ACEI increased the left ventricular (LV) ejection fraction and reduced LV chamber dimension and mass, but these effects were attenuated in B 2 receptor knockout mice. 4 In the clinical setting, however, the majority of patients with what is currently called "systolic heart failure" also have diastolic dysfunction of various degrees. 5 Ang II affects diastolic LV function through the changed composition of the LV wall (ie, increased interstitial fibrosis or fibrous content) and by virtue of the altered activity of the myofibroblasts in CHF. Because BK also possesses antiproliferative propertie...

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Section: Discussioncontrasting

confidence: 56%

Bradykinin Improves Left Ventricular Diastolic Function Under Long-Term Angiotensin-Converting Enzyme Inhibition in Heart Failure

et al. 2002

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“…In most cases there is expression of a fetal isoform in the disease state [16,65,82,84,[86][87][88][89]. Isoform variation of TnT is the result of alternative splicing of a single gene product, specifically 15 and/or 30 nt exons in the glutamate rich, highly charged N terminal segment [82,[90][91][92]. Anderson and colleagues first reported a TnT isoform shift in human heart failure in both non-ischemic and ischemic heart failure.…”

Section: Tnt Isoform Shiftsmentioning

confidence: 98%

Thin Filament Remodeling in Failing Myocardium

VanBuren

Okada

2005

Heart Fail Rev

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While the remodeling process in myocardial failure involves changes in ventricular structure and performance, it is now appreciated that it is also associated with changes in thin filament composition and function. As is discussed, changes at the level thick filament may affect thin filament activation in heart failure. Alterations in actin, troponin and tropomyosin isoform composition do not appear to be significant factors in human heart failure. In contrast, proteolytic degradation of troponin subunits are likely to be playing a functional role in some forms of cardiomyopathy (e.g. ischemic). Finally, phosphorylation of troponin I and troponin T by kinases (most notably protein kinase C) substantially affect thin filament function in failing human myocardium. These findings indicate that functional deficits in thin filament function in failing myocardium are largely reversible and create the potential for future targeted therapies in the treatment of this deadly disease.

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“…Treatment of rats with different angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor (AT1R) antagonists has been shown to prevent ventricular remodelling, improve heart function, change hormone profile and reduce mortality in the infarcted animals [18][19][20][21][22]. Although the cellular and molecular mechanisms by which these drugs improve cardiac function in heart failure have not yet been clearly defined, Shao et al [23] have demonstrated the effect of ACE inhibition on sarcoplasmic reticular gene expression whereas Wang et al [24] demonstrated that the beneficial effects on the failing heart are associated with prevention of changes in myosin heavy chain isozyme protein contents and gene expression. Furthermore, recently the role of RAS in the phospholipase C-mediated signalling in congestive heart failure (CHF) has also been suggested [25].…”

Section: Introductionmentioning

confidence: 99%

Attenuation of changes in G_i‐proteins and adenylyl cyclase in heart failure by an ACE inhibitor, imidapril

Sethi

Shao

Takeda

et al. 2003

J Cellular Molecular Medi

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Cardiac dysfunction in animals with congestive heart failure due to myocardial infarction (MI) is known to be associated with a wide variety of defects in receptor and post-receptor mechanisms. Since the heart function have been shown to be improved by treatment with different angiotensin converting enzyme (ACE) inhibitors, we examined the effects of imidapril, an ACE inhibitor, on changes in post-receptor mechanisms involving adenylyl cyclase (AC) and G proteins in the failing heart. Heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated daily with 1 mg/kg (orally) imidapril for 5 weeks. The animals were assessed for their left ventricular function and crude membranes were isolated from the viable left ventricle and examined for AC activities as well as G-protein activities and expression. Animals with heart failure exhibited depressions in ventricular function and AC activities in the absence or presence of forskolin, NaF and Gpp(NH)p. The AC activity in the presence of pertussis toxin was increased whereas that in the presence of cholera toxin was decreased in the failing heart. Protein contents and mRNA levels for G i -proteins were increased whereas those for G s -proteins were unaltered in the infarcted heart. All these changes due to MI were prevented by imidapril treatment. The results indicate that the depressed cardiac function in the failing heart may partly be due to the direct effects of changes in AC and G i proteins.

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Captopril Treatment Improves the Sarcoplasmic Reticular Ca2+Transport in Heart Failure Due to Myocardial Infarction

Cited by 35 publications

References 30 publications

Bradykinin Improves Left Ventricular Diastolic Function Under Long-Term Angiotensin-Converting Enzyme Inhibition in Heart Failure

Bradykinin Improves Left Ventricular Diastolic Function Under Long-Term Angiotensin-Converting Enzyme Inhibition in Heart Failure

Thin Filament Remodeling in Failing Myocardium

Attenuation of changes in G_i‐proteins and adenylyl cyclase in heart failure by an ACE inhibitor, imidapril

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Captopril Treatment Improves the Sarcoplasmic Reticular Ca2+Transport in Heart Failure Due to Myocardial Infarction

Cited by 35 publications

References 30 publications

Bradykinin Improves Left Ventricular Diastolic Function Under Long-Term Angiotensin-Converting Enzyme Inhibition in Heart Failure

Bradykinin Improves Left Ventricular Diastolic Function Under Long-Term Angiotensin-Converting Enzyme Inhibition in Heart Failure

Thin Filament Remodeling in Failing Myocardium

Attenuation of changes in Gi‐proteins and adenylyl cyclase in heart failure by an ACE inhibitor, imidapril

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Attenuation of changes in G_i‐proteins and adenylyl cyclase in heart failure by an ACE inhibitor, imidapril