Journal of cardiovascular pharmacology · 2012
Different roles of PPAR-γ activity on physiological and pathological alteration after myocardial ischemia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Nagashima Ayako, Watanabe Ryo, Ogawa Masahito, Suzuki Jun-Ichi, Masumura Mayumi, Hishikari Keiichi, Shimizu Tomoko, Takayama Kiyoshi, Hirata Yasunobu, Nagai Ryozo, Isobe Mitsuaki
Аннотация
BACKGROUND: Telmisartan is an angiotensin II receptor blocker, which acts as a partial agonist of peroxisome proliferator activator receptor-γ (PPAR-γ). Because PPAR-γ initiates a variety of antiinflammatory responses, the effect on myocardial ischemia is to be elucidated.
METHODS AND RESULTS: The left anterior descending arteries were ligated to induce myocardial infarction in rats. The animals were assigned to 4 groups: (1) control (saline, n = 6), (2) telmisartan (10 mg·kg·d, n = 6), (3) telmisartan + GW9662 (PPAR-γ-antagonist) (10 mg·kg·d of telmisartan and 1 mg·kg·d of GW9662, n = 6), and (4) amlodipine (10 mg·kg·d, n = 8) groups. Telmisartan reduced mean blood pressure compared with that in the control group. There was no statistical difference among the telmisartan, telmisartan + GW9662 and amlodipine groups. The end-diastolic left ventricular diameter was smaller in telmisartan group compared with that in the control group; GW9662 negated the effect of telmisartan. The thickness of the ventricular septum was kept in the telmisartan group compared with that in the control group; GW9662 negated the effect. Histopathologic analyses showed that telmisartan suppressed myocardial fibrosis compared with that of the control, whereas GW9662 negated the telmisartan effect.
CONCLUSIONS: Telmisartan suppresses pathological remodeling by PPAR-γ agonistic activities independent of its antihypertensive effects.
METHODS AND RESULTS: The left anterior descending arteries were ligated to induce myocardial infarction in rats. The animals were assigned to 4 groups: (1) control (saline, n = 6), (2) telmisartan (10 mg·kg·d, n = 6), (3) telmisartan + GW9662 (PPAR-γ-antagonist) (10 mg·kg·d of telmisartan and 1 mg·kg·d of GW9662, n = 6), and (4) amlodipine (10 mg·kg·d, n = 8) groups. Telmisartan reduced mean blood pressure compared with that in the control group. There was no statistical difference among the telmisartan, telmisartan + GW9662 and amlodipine groups. The end-diastolic left ventricular diameter was smaller in telmisartan group compared with that in the control group; GW9662 negated the effect of telmisartan. The thickness of the ventricular septum was kept in the telmisartan group compared with that in the control group; GW9662 negated the effect. Histopathologic analyses showed that telmisartan suppressed myocardial fibrosis compared with that of the control, whereas GW9662 negated the telmisartan effect.
CONCLUSIONS: Telmisartan suppresses pathological remodeling by PPAR-γ agonistic activities independent of its antihypertensive effects.
Предметные рубрики MeSH
AmlodipineAngiotensin II Type 1 Receptor BlockersAnilidesAnimalsAntihypertensive AgentsBenzimidazolesBenzoatesBlood PressureCalcium Channel BlockersCells, CulturedDisease Models, AnimalDrug Partial AgonismFibrosisHypertrophy, Left VentricularMaleMatrix Metalloproteinase 2Myocardial InfarctionMyocardiumPPAR gammaPioglitazoneRatsRats, Sprague-DawleyStroke VolumeTelmisartanThiazolidinedionesTime FactorsVentricular Function, LeftVentricular Remodeling