Prevention of the development of heart failure and the regression of cardiac hypertrophy by captopril in the spontaneously hypertensive rat

1983 ◽  
Vol 4 (suppl A) ◽  
pp. 143-148 ◽  
Author(s):  
J. M. Pfeffer ◽  
M. A. Pfeffer ◽  
I. Mirsky ◽  
E. Braunwald
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Regression Of Cardiac Hypertrophy

Phosphorylation of RyR2 and shortening of RyR2 cluster spacing in spontaneously hypertensive rat with heart failure

2007 ◽  
Vol 293 (4) ◽  
pp. H2409-H2417 ◽  
Author(s):  
Ye Chen-Izu ◽  
Christopher W. Ward ◽  
Wayne Stark ◽  
Tamas Banyasz ◽  
Marius P. Sumandea ◽  
...  
Keyword(s):  
Heart Failure ◽  
Spontaneously Hypertensive Rat ◽  
Model Simulation ◽  
Quantitative Model ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Distinct Disease ◽  
Intracellular Ca ◽  
Disease Stages

As a critical step toward understanding the role of abnormal intracellular Ca2+ release via the ryanodine receptor (RyR2) during the development of hypertension-induced cardiac hypertrophy and heart failure, this study examines two questions: 1) At what stage, if ever, in the development of hypertrophy and heart failure is RyR2 hyperphosphorylated at Ser2808? 2) Does the spatial distribution of RyR2 clusters change in failing hearts? Using a newly developed semiquantitative immunohistochemistry method and Western blotting, we measured phosphorylation of RyR2 at Ser2808 in the spontaneously hypertensive rat (SHR) at four distinct disease stages. A major finding is that hyperphosphorylation of RyR2 at Ser2808 occurred only at late-stage heart failure in SHR, but not in age-matched controls. Furthermore, the spacing between RyR2 clusters was shortened in failing hearts, as predicted by quantitative model simulation to increase spontaneous Ca2+ wave generation and arrhythmias.

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