Contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats

1999 ◽  
Vol 97 (2) ◽  
pp. 239 ◽  
Author(s):  
Shuntaro IKEDA ◽  
Mareomi HAMADA ◽  
Kunio HIWADA
Keyword(s):  
Heart Failure ◽  
Spontaneously Hypertensive Rats ◽  
Cardiomyocyte Apoptosis ◽  
Cardiac Remodelling ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats

1999 ◽  
Vol 97 (2) ◽  
pp. 239-246 ◽  
Author(s):  
Shuntaro IKEDA ◽  
Mareomi HAMADA ◽  
Kunio HIWADA
Keyword(s):  
Heart Failure ◽  
Spontaneously Hypertensive Rats ◽  
Wall Stress ◽  
Decompensated Heart Failure ◽  
Cardiomyocyte Apoptosis ◽  
Cardiac Remodelling ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Systolic Wall Stress ◽  
Fractional Shortening

Various alterations in molecular and cellular events have been considered as possibly contributing to the cardiac remodelling that occurs during the transition from compensated hypertrophy to heart failure. The aim of the present study is to clarify (1) whether cardiac apoptosis occurs during the transition from compensated hypertrophy to decompensated heart failure, and (2) whether expression of the genes encoding Bax (an apoptosis inducer) and Bcl-xL and Bcl-2 (apoptosis inhibitors) is altered during this transition. We used 12-month-old and 20-month-old male spontaneously hypertensive rats (SHR12 and SHR20 respectively) and age-matched Wistar–Kyoto rats (WKY12 and WKY20 respectively). These rats were killed after measurement of haemodynamic parameters by transthoracic echocardiography and use of a tipmanometer via the right carotid artery. The expression of bcl-2, bcl-xL and bax was analysed by Northern blotting. Samples were also fixed in 4% paraformaldehyde for in situ nick end-labelling (TUNEL) methods and immunohistochemistry. SHR12 had well compensated left ventricular hypertrophy with normal fractional shortening and normal end-systolic wall stress. In contrast, the hearts of SHR20 developed decompensated dilatation, with a decrease in fractional shortening and an increase in end-systolic wall stress. TUNEL-positive cells were seen exclusively in the hearts of SHR20. The major cell types that showed TUNEL-positive nuclei were non-cardiomyocytes. The expression of bax remained unchanged during the transition to heart failure. However, there was increased expression of bcl-xL in the failing stage, whereas the expression of bcl-2 remained unchanged. Immunohistochemical studies revealed that Bcl-xL protein was up-regulated in the hearts of SHR20. In conclusion, non-cardiomyocyte apoptosis may play a contributory role in the remodelling that occurs in the transition from compensatory hypertrophy to decompensated heart failure. In addition, it is suggested that enhanced expression of bcl-xL plays an important role in the preservation of cardiomyocytes during this transition.

Cardiomyocyte Apoptosis and Cardiac Angiotensin-Converting Enzyme in Spontaneously Hypertensive Rats

Hypertension ◽  
1997 ◽  
Vol 30 (5) ◽  
pp. 1029-1034 ◽  
Author(s):  
Javier Díez ◽  
Angel Panizo ◽  
Marta Hernández ◽  
Francisco Vega ◽  
Iosu Sola ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Spontaneously Hypertensive Rats ◽  
Cardiomyocyte Apoptosis ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Heart failure-induced skeletal myopathy in spontaneously hypertensive rats

2013 ◽  
Vol 167 (3) ◽  
pp. 698-703 ◽  
Author(s):  
R.L. Damatto ◽  
P.F. Martinez ◽  
A.R.R. Lima ◽  
M.D.M. Cezar ◽  
D.H.S. Campos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Skeletal Myopathy
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