Differences in Concentric Cardiac Hypertrophy and Eccentric Hypertrophy

2012 ◽  
pp. 147-166 ◽  
Author(s):  
Alison L. Müller ◽  
Naranjan S. Dhalla
Keyword(s):  
Cardiac Hypertrophy ◽  
Eccentric Hypertrophy

Regulation of atrial contraction by PKA and PKC during development and regression of eccentric cardiac hypertrophy

2005 ◽  
Vol 288 (2) ◽  
pp. H695-H704 ◽  
Author(s):  
Georges E. Haddad ◽  
Bernell R. Coleman ◽  
Aiqiu Zhao ◽  
Krista N. Blackwell
Keyword(s):  
Cardiac Hypertrophy ◽  
Left Atrial ◽  
Ace Inhibitor ◽  
Ace Inhibition ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Tissue Mass ◽  
Peak Tension ◽  
Eccentric Hypertrophy ◽  
Differential Responsiveness

ANG II plays a major role in development of cardiac hypertrophy through its AT1 receptor subtype, whereas angiotensin-converting enzyme (ACE) inhibitors are effective in reversing effects of ANG II on the heart. The objective of this study was to investigate the role of PKA and PKC in the contractile response of atrial tissue during development and ACE inhibitor-induced regression of eccentric hypertrophy induced by aortocaval shunt. At 1 wk after surgery, sham and shunt rats were divided into captopril-treated and untreated groups for 2 wk. Then isometric contraction was assessed by electrical stimulation of isolated rat left atrial preparations superfused with Tyrode solution in the presence or absence of specific inhibitors KT-5720 (for PKA) and Ro-32-0432 (for PKC) and high Ca2+. Peak tension developed was greater in shunt than in sham hearts. However, when expressed relative to tissue mass, hypertrophied muscle showed weaker contraction than muscle from sham rats. In sham rats, peak tension developed was more affected by PKC than by PKA inhibition, whereas this differential effect was reduced in the hypertrophied heart. Treatment of shunt rats with captopril regressed left atrial hypertrophy by 67% and restored PKC-PKA differential responsiveness toward sham levels. In the hypertrophied left atria, there was an increase in the velocity of contraction and relaxation that was not evident when expressed in specific relative terms. Treatment with ACE inhibitor increased the specific velocity of contraction, as well as its PKC sensitivity, in shunt rats. We conclude that ACE inhibition during eccentric cardiac hypertrophy produces a negative trophic and a positive inotropic effect, mainly through a PKC-dependent mechanism.

scholarly journals Herbal Supplement Ameliorates Cardiac Hypertrophy in Rats with CCl4-Induced Liver Cirrhosis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Ping-Chun Li ◽  
Yung-Wei Chiu ◽  
Yueh-Min Lin ◽  
Cecilia Hsuan Day ◽  
Guang-Yuh Hwang ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Cardiac Hypertrophy ◽  
Signaling Pathway ◽  
Herbal Supplement ◽  
Herbal Supplements ◽  
Cardiac Tissues ◽  
Expression Of Genes ◽  
Eccentric Hypertrophy ◽  
Male Wistar Rats ◽  
Molecular Mechanism Of Action

We used the carbon tetrachloride (CCl4) induced liver cirrhosis model to test the molecular mechanism of action involved in cirrhosis-associated cardiac hypertrophy and the effectiveness of Ocimum gratissimum extract (OGE) and silymarin against cardiac hypertrophy. We treated male wistar rats with CCl4 and either OGE (0.02 g/kg B.W. or 0.04 g/kg B.W.) or silymarin (0.2 g/kg B.W.). Cardiac eccentric hypertrophy was induced by CCl4 along with cirrhosis and increased expression of cardiac hypertrophy related genes NFAT, TAGA4, and NBP, and the interleukin-6 (IL-6) signaling pathway related genes MEK5, ERK5, JAK, and STAT3. OGE or silymarin co-treatment attenuated CCl4-induced cardiac abnormalities, and lowered expression of genes which were elevated by this hepatotoxin. Our results suggest that the IL-6 signaling pathway may be related to CCl4-induced cardiac hypertrophy. OGE and silymarin were able to lower liver fibrosis, which reduces the chance of cardiac hypertrophy perhaps by lowering the expressions of IL-6 signaling pathway related genes. We conclude that treatment of cirrhosis using herbal supplements is a viable option for protecting cardiac tissues against cirrhosis-related cardiac hypertrophy.

scholarly journals Effects of Trandolapril on Structural, Contractile and Electrophysiological Remodeling in Experimental Volume Overload Heart Failure

2021 ◽  
Vol 12 ◽  
Author(s):  
Dagmar Jarkovská ◽  
Matúš Miklovič ◽  
Jitka Švíglerová ◽  
Luděk Červenka ◽  
Petra Škaroupková ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Volume Overload ◽  
Ace Inhibition ◽  
Therapeutic Effects ◽  
Aortocaval Shunt ◽  
Needle Technique ◽  
Chronic Volume Overload ◽  
Eccentric Hypertrophy

Chronic volume overload induces multiple cardiac remodeling processes that finally result in eccentric cardiac hypertrophy and heart failure. We have hypothesized that chronic angiotensin-converting enzyme (ACE) inhibition by trandolapril might affect various remodeling processes differentially, thus allowing their dissociation. Cardiac remodeling due to chronic volume overload and the effects of trandolapril were investigated in rats with an aortocaval fistula (ACF rats). The aortocaval shunt was created using a needle technique and progression of cardiac remodeling to heart failure was followed for 24 weeks. In ACF rats, pronounced eccentric cardiac hypertrophy and contractile and proarrhythmic electrical remodeling were associated with increased mortality. Trandolapril substantially reduced the electrical proarrhythmic remodeling and mortality, whereas the effect on cardiac hypertrophy was less pronounced and significant eccentric hypertrophy was preserved. Effective suppression of electrical proarrhythmic remodeling and mortality but not hypertrophy indicates that the beneficial therapeutic effects of ACE inhibitor trandolapril in volume overload heart failure might be dissociated from pure antihypertrophic effects.

Probiotic Escherichia coli Nissle inhibits IL-6 and MAPK-mediated cardiac hypertrophy during STZ-induced diabetes in rats

2021 ◽  
pp. 1-12
Author(s):  
C.J. Chiang ◽  
Y.P. Chao ◽  
A. Ali ◽  
C.H. Day ◽  
T.J. Ho ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cardiac Hypertrophy ◽  
Diabetic Rats ◽  
Probiotic Bacterium ◽  
Oral Gavage ◽  
Mapk Signalling ◽  
Signalling Cascades ◽  
Eccentric Hypertrophy ◽  
Cardioprotective Effects ◽  
Escherichia Coli Nissle

Escherichia coli Nissle (EcN), a probiotic bacterium protects against several disorders. Multiple reports have studied the pathways involved in cardiac hypertrophy. However, the effects of probiotic EcN against diabetes-induced cardiac hypertrophy remain to be understood. We administered five weeks old Wistar male (271±19.4 g body weight) streptozotocin-induced diabetic rats with 109 cfu of EcN via oral gavage every day for 24 days followed by subjecting the rats to echocardiography to analyse the cardiac parameters. Overexpressed interleukin (IL)-6 induced the MEK5/ERK5, JAK2/STAT3, and MAPK signalling cascades in streptozotocin-induced diabetic rats. Further, the upregulation of calcineurin, NFATc3, and p-GATA4 led to the elevation of hypertrophy markers, such as atrial and B-type natriuretic peptides. In contrast, diabetic rats supplemented with probiotic EcN exhibited significant downregulated IL-6. Moreover, the MEK5/ERK5 and JAK2/STAT3 cascades involved during eccentric hypertrophy and MAPK signalling, including phosphorylated MEK, ERK, JNK, and p-38, were significantly attenuated in diabetic rats after supplementation of EcN. Western blotting and immunofluorescence revealed the significant downregulation of NFATc3 and downstream mediators, thereby resulting in the impairment of cardiac hypertrophy. Taken together, the findings demonstrate that supplementing probiotic EcN has the potential to show cardioprotective effects by inhibiting diabetes-induced cardiomyopathies.

Regulation of insulin-like growth factor-1 by the renin–angiotensin system during regression of cardiac eccentric hypertrophy through angiotensin-converting enzyme inhibitor and AT1 antagonist

2003 ◽  
Vol 81 (2) ◽  
pp. 142-149 ◽  
Author(s):  
G E Haddad ◽  
K Blackwell ◽  
A Bikhazi
Keyword(s):  
Growth Factor ◽  
Angiotensin Converting Enzyme ◽  
Cardiac Hypertrophy ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Eccentric Hypertrophy ◽  
Regression Of Cardiac Hypertrophy

Angiotensin II (Ang II) mediates its effects through its non-tyrosine-kinase G protein coupled Ang-II type 1 receptor (AT1). Growing evidence indicates that a functional insulin-like growth factor-1 (IGF-1) tyrosine kinase receptor is required for Ang-II-induced mitogenesis. Along with Ang II, we have previously shown that changes in IGF-1 receptor binding at myofibers are causative agents for cardiac eccentric hypertrophy. This study investigated the interaction of the renin–angiotensin system with the IGF-1 receptor during the development and regression of cardiac hypertrophy. Alterations in IGF-1 binding were evaluated in the CHAPS-pretreated perfused heart. Four weeks of aortocaval shunt increased relative heart mass by 76% without a major change in body mass or systolic blood pressure. Binding studies showed that IGF-1 has a higher affinity for the cardiac myofibers of shunt than sham rats. Two weeks of treatment with the angiotensin-converting enzyme (ACE) inhibitor captopril (0.5 g/L in drinking water) or the AT1-antagonist losartan (10 mg/(kg·day)) reduced cardiac hypertrophy by 54 and 42%, respectively. However, while both ACE inhibition and AT1-antagonist treatments produced equivalent regression in ventricular hypertrophy, captopril was more efficacious than losartan in the regression of atrial hypertrophy. Regression of cardiac hypertrophy in the shunt by either captopril or losartan was accompanied with a reduction or normalization of the elevated IGF-1 affinity. Thus, the induction and regression of cardiac eccentric hypertrophy seems to be largely dependent on cross talk between the renin–angiotensin system and the IGF-1 axis at the receptor level.Key words: volume overload, cardiac eccentric hypertrophy, renin–angiotensin system, IGF-1.

421 The NFATc2 isoform plays a major role in calcineurin-induced cardiac hypertrophy

2006 ◽  
Vol 5 (1) ◽  
pp. 98-98
Author(s):  
M BOURAJJAJ ◽  
A ARMAND ◽  
B WEIJTS ◽  
L DEWINDT
Keyword(s):  
Cardiac Hypertrophy

Sex differences in cardiac hypertrophy are linked to adipose tissue lipolysis

2011 ◽  
Vol 6 (S 01) ◽  
Author(s):  
A Foryst-Ludwig ◽  
M Kreissl ◽  
C Sprang ◽  
B Thalke ◽  
C Böhm ◽  
...  
Keyword(s):  
Sex Differences ◽  
Adipose Tissue ◽  
Cardiac Hypertrophy ◽  
Adipose Tissue Lipolysis
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