Histone Deacetylase Inhibition Attenuates Cardiac Hypertrophy and Fibrosis through Acetylation of Mineralocorticoid Receptor in Spontaneously Hypertensive Rats

2015 ◽  
Vol 87 (5) ◽  
pp. 782-791 ◽  
Author(s):  
Seol-Hee Kang ◽  
Young Mi Seok ◽  
Min-ji Song ◽  
Hae-Ahm Lee ◽  
Thomas Kurz ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Histone Deacetylase ◽  
Mineralocorticoid Receptor ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Histone Deacetylase Inhibition ◽  
Spontaneously Hypertensive

scholarly journals Continuous Blockade of L-Type Ca2+ Channels Suppresses Activation of Calcineurin and Development of Cardiac Hypertrophy in Spontaneously Hypertensive Rats

2002 ◽  
Vol 25 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Yunzeng ZOU ◽  
Tsutomu YAMAZAKI ◽  
Keiichi NAKAGAWA ◽  
Haruyasu YAMADA ◽  
Norio IRIGUCHI ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ca2 Channels

Ca2+/calmodulin-dependent protein kinase II increases the susceptibility to the arrhythmogenic action potential alternans in spontaneously hypertensive rats

2014 ◽  
Vol 307 (2) ◽  
pp. H199-H206 ◽  
Author(s):  
Hirofumi Mitsuyama ◽  
Hisashi Yokoshiki ◽  
Masaya Watanabe ◽  
Kazuya Mizukami ◽  
Junichi Shimokawa ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Action Potential ◽  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Dependent Protein Kinase ◽  
Spontaneously Hypertensive ◽  
Dependent Protein ◽  
Rapid Pacing ◽  
Increased Susceptibility

Action potential duration alternans (APD-ALT), defined as long-short-long repetitive pattern of APD, potentially leads to lethal ventricular arrhythmia. However, the mechanisms of APD-ALT in the arrhythmogenesis of cardiac hypertrophy remain undetermined. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is known to modulate the function of cardiac sarcoplasmic reticulum and play an important role in Ca2+ cycling. We thus aimed to determine the role of CaMKII in the increased susceptibility to APD-ALT and arrhythmogenesis in the hypertrophied heart. APD was measured by high-resolution optical mapping in left ventricular (LV) anterior wall from normotensive Wistar-Kyoto (WKY; n = 10) and spontaneously hypertensive rats (SHR; n = 10) during rapid ventricular pacing. APD-ALT was evoked at significantly lower pacing rate in SHR compared with WKY (382 ± 43 vs. 465 ± 45 beats/min, P < 0.01). These changes in APD-ALT in SHR were completely reversed by KN-93 (1 μmol/l; n = 5), an inhibitor of CaMKII, but not its inactive analog, KN-92 (1 μmol/l; n = 5). The magnitude of APD-ALT was also significantly greater in SHR than WKY and was completely normalized by KN-93. Ventricular fibrillation (VF) was induced by rapid pacing more frequently in SHR than in WKY (60 vs. 10%; P < 0.05), which was also abolished by KN-93 (0%, P < 0.05). Western blot analyses indicated that the CaMKII autophosphorylation at Thr287 was significantly increased in SHR compared with WKY. The increased susceptibility to APD-ALT and VF during rapid pacing in hypertrophied heart was prevented by KN-93. CaMKII could be an important mechanism of arrhythmogenesis in cardiac hypertrophy.

scholarly journals Apoptosis During Regression of Cardiac Hypertrophy in Spontaneously Hypertensive Rats

Hypertension ◽  
1999 ◽  
Vol 34 (2) ◽  
pp. 229-235 ◽  
Author(s):  
Bun-Seng Tea ◽  
Than-Vinh Dam ◽  
Pierre Moreau ◽  
Pavel Hamet ◽  
Denis deBlois
Keyword(s):  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Regression Of Cardiac Hypertrophy
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