Ultrastructural changes during myocardial hypertrophy and its regression: Long-term effects of nifedipine in adult spontaneously hypertensive rats

1997 ◽  
Vol 12 (3) ◽  
pp. 143-151 ◽  
Author(s):  
Toshiyuki Kimpara ◽  
Makoto Okabe ◽  
Hikaru Nishimura ◽  
Tetsuya Hayashi ◽  
Kikuko Imamura ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Myocardial Hypertrophy ◽  
Ultrastructural Changes ◽  
Long Term Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Long-term effects of the PPARγ activator pioglitazone on cardiac inflammation in stroke-prone spontaneously hypertensive rats

2004 ◽  
Vol 82 (11) ◽  
pp. 976-985 ◽  
Author(s):  
Quy N Diep ◽  
Farhad Amiri ◽  
Karim Benkirane ◽  
Pierre Paradis ◽  
Ernesto L Schiffrin
Keyword(s):  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Genetic Model ◽  
Left Ventricular ◽  
Long Term Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cardiac Inflammation ◽  
Pioglitazone Treatment

We investigated the long-term effects of the thiazolidinedione PPARγ activator pioglitazone on cardiac inflammation in stroke-prone spontaneously hypertensive rats (SHRSP), a model of malignant of hypertension. Six-week-old SHRSP were treated with pioglitazone (10 mg/kg per day p.o.) for 20 weeks. The rise in systolic blood pressure (SBP) in SHRSP was only transiently and slightly attenuated by pioglitazone (P < 0.05). On one hand, cardiac hypertrophy was little affected by the pioglitazone treatment, and there was only a reduction of subepicardial interstitial fibrosis. On the other hand, left ventricular NFκB and AP-1 binding activities, the expression of TNFα, and the adhesion of molecule PECAM were significantly decreased by pioglitazone treatment. Expression of the pro-apoptotic proteins p53 and bax was significantly increased by pioglitazone. Thus, pioglitazone-attenuated cardiac inflammation in SHRSP had little effect on BP or cardiac hypertrophy. PPARγ activation may play a preventive cardiovascular role by offsetting the cardiac inflammatory response as demonstrated in this genetic model of malignant hypertension.Key words: hypertension, heart, inflammation, NFκB, adhesion molecules.

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