Document Detail


Different roles of PPAR-γ activity on physiological and pathological alteration after myocardial ischemia.
MedLine Citation:
PMID:  22561360     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Ayako Nagashima; Ryo Watanabe; Masahito Ogawa; Jun-Ichi Suzuki; Mayumi Masumura; Keiichi Hishikari; Tomoko Shimizu; Kiyoshi Takayama; Yasunobu Hirata; Ryozo Nagai; Mitsuaki Isobe
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  60     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-15     Completed Date:  2012-12-26     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  158-64     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Amlodipine / pharmacology
Angiotensin II Type 1 Receptor Blockers / pharmacology*
Anilides / pharmacology
Animals
Antihypertensive Agents / pharmacology
Benzimidazoles / pharmacology*
Benzoates / pharmacology*
Blood Pressure / drug effects
Calcium Channel Blockers / pharmacology
Cells, Cultured
Disease Models, Animal
Drug Partial Agonism
Fibrosis
Hypertrophy, Left Ventricular / metabolism,  pathology,  physiopathology,  prevention & control
Male
Matrix Metalloproteinase 2 / metabolism
Myocardial Infarction / drug therapy*,  metabolism,  pathology,  physiopathology
Myocardium / metabolism*,  pathology
PPAR gamma / agonists*,  antagonists & inhibitors,  metabolism
Rats
Rats, Sprague-Dawley
Stroke Volume / drug effects
Thiazolidinediones / pharmacology
Time Factors
Ventricular Function, Left / drug effects
Ventricular Remodeling / drug effects
Chemical
Reg. No./Substance:
0/2-chloro-5-nitrobenzanilide; 0/Angiotensin II Type 1 Receptor Blockers; 0/Anilides; 0/Antihypertensive Agents; 0/Benzimidazoles; 0/Benzoates; 0/Calcium Channel Blockers; 0/PPAR gamma; 0/Thiazolidinediones; 1J444QC288/Amlodipine; EC 3.4.24.24/Matrix Metalloproteinase 2; EC 3.4.24.24/Mmp2 protein, rat; U5SYW473RQ/telmisartan; X4OV71U42S/pioglitazone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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