Early relief of aortic coarctation results in complete regression of cardiac hypertrophy and associated changes in the transcriptome; an animal model

2015 ◽  
Vol 24 ◽  
pp. S177
Author(s):  
S. Chen ◽  
D. Drak ◽  
A. Krishnan ◽  
W. Li ◽  
G. Denyer ◽  
...  
Keyword(s):  
Animal Model ◽  
Cardiac Hypertrophy ◽  
Aortic Coarctation ◽  
Complete Regression ◽  
Regression Of Cardiac Hypertrophy

Alteration of Atrial Natriuretic Peptide and Brain Natriuretic Peptide Gene Expression Associated with Progression and Regression of Cardiac Hypertrophy in Renovascular Hypertensive Rats

1996 ◽  
Vol 90 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Hideo Kawakami ◽  
Hideki Okayama ◽  
Mareomi Hamada ◽  
Kunio Hiwada
Keyword(s):  
Gene Expression ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Regression Of Cardiac Hypertrophy ◽  
Peptide Gene ◽  
Atrial Natriuretic

1. We assessed the changes of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats (RHR). 2. Two-kidney, one-clip hypertensive rats (6-week-old male Wistar) were made and studied 6 (RHR-1) and 10 weeks (RHR-2) after the procedure. Regression of cardiac hypertrophy was induced by nephrectomy at 6 weeks after constriction, and the nephrectomized rats were maintained further for 4 weeks (nephrectomized rat: NEP). Sham operation was performed, and the rats were studied after 6 (Sham-1) and 10 weeks (Sham-2). Atrial natriuretic peptide and brain natriuretic peptide gene expression in the left ventricle was analysed by Northern blotting. 3. Plasma atrial natriuretic peptide and brain natriuretic peptide were significantly higher in RHR-1 and RHR-2 than in Sham-1, Sham-2 and NEP. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in RHR-1 were approximately 7.2-fold and 1.8-fold higher than those in Sham-1, respectively, and the corresponding levels in RHR-2 were 13.0-fold and 2.4-fold higher than those in Sham-2, respectively. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels of NEP were normalized. Levels of atrial natriuretic peptide and brain natriuretic peptide mRNA were well correlated positively with left ventricular weight/body weight ratios. There was a significant positive correlation between the levels of atrial natriuretic peptide and brain natriuretic peptide mRNA (r = 0.86, P<0.01). 4. We conclude that the expression of atrial natriuretic peptide and brain natriuretic peptide genes is regulated in accordance with the degree of myocardial hypertrophy and that the augmented expression of these two natriuretic peptides may play an important role in the maintenance of cardiovascular haemodynamics in renovascular hypertension.

Hyperactivation of mTORC1 in a Cardiac Hypertrophy Animal Model of Friedreich's Ataxia

2021 ◽  
Author(s):  
Wing-Hang Tong ◽  
Hayden Ollivierre ◽  
Audrey Noguchi ◽  
Manik Ghosh ◽  
Danielle A. Springer ◽  
...  
Keyword(s):  
Animal Model ◽  
Cardiac Hypertrophy ◽  
Friedreich’S Ataxia ◽  
Friedreich's Ataxia

scholarly journals Calcineurin Inhibitor Attenuates the Development and Induces the Regression of Cardiac Hypertrophy in Rats With Salt-Sensitive Hypertension

Circulation ◽  
2000 ◽  
Vol 102 (16) ◽  
pp. 1996-2004 ◽  
Author(s):  
Masaki Shimoyama ◽  
Doubun Hayashi ◽  
Yunzeng Zou ◽  
Eiki Takimoto ◽  
Miho Mizukami ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Calcineurin Inhibitor ◽  
Regression Of Cardiac Hypertrophy ◽  
Salt Sensitive Hypertension

Humoral factor(s) produced by pressure overload enhance cardiac hypertrophy and natriuretic peptide expression

1997 ◽  
Vol 273 (1) ◽  
pp. H113-H118 ◽  
Author(s):  
T. Iso ◽  
M. Arai ◽  
A. Wada ◽  
K. Kogure ◽  
T. Suzuki ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Aortic Coarctation ◽  
Pressure Overload ◽  
Humoral Factor ◽  
Myosin Isoforms ◽  
Hypertrophic Response ◽  
Cardiac Atrophy ◽  
Transplanted Hearts

Chronic pressure overload is known to increase cardiac mass and expression levels of both atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNAs. Although mechanical stretching of cardiac myocytes could cause these changes, humoral factor(s) secondary to pressure overload may also be involved. To dissociate humoral effects from the effects of mechanical loading on cardiac hypertrophic responses, we examined expression of ANP and BNP at both mRNA and protein levels and proportions of myosin isoforms in transplanted cervical hearts that were mechanically unloaded under conditions with or without hypertension by aortic coarctation. Seven days after transplantation, cardiac atrophy that usually occurs in transplanted hearts without hypertension by coarctation was prevented in the transplanted hearts with hypertension by coarctation. The levels of expression of ANP and BNP mRNAs were increased in the transplanted hearts with relative to those without hypertension by coarctation. The plasma level of angiotensin II was higher in rats with than without hypertension by coarctation. Plasma endothelin-1 levels were not significantly different between the two groups. In addition, levels of expression of ANP and BNP mRNAs were increased in the transplanted hearts without hypertension relative to those in the in situ hearts. The proportion of the V3 myosin isoform was also increased in the transplanted hearts without hypertension relative to the in situ hearts. These results indicate that humoral factor(s) secondary to the pressure overload produced by aortic coarctation enhanced the cardiac hypertrophic response and elevated the levels of mRNAs encoding these embryonic markers. Moreover, our findings regarding ANP and BNP expression in the transplanted hearts provide additional evidence that the fetal genes are reexpressed during the process of cardiac atrophy as well as in cardiac hypertrophy.

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