title: Telmisartan attenuates myocardial apoptosis induced by chronic intermittent hypoxia in rats: modulation of nitric oxide metabolism and inflammatory mediators.
abstract: OBJECTIVE
  NO and NO synthase (NOS) are known to play key roles in the development of myocardial apoptosis induced by ischemia/hypoxia. Current evidence suggests that angiotensin II type 1 receptor blockers, such as telmisartan, lower blood pressure and produce beneficial regulatory effects on NO and NOS. Here, we examined the protective role of telmisartan in myocardial apoptosis induced by chronic intermittent hypoxia (CIH).
  
  
  METHODS
  Adult male Sprague-Dawley rats were subjected to 8 h of intermittent hypoxia/day, with/without telmisartan for 8 weeks. Myocardial apoptosis, NO and NOS activity, and levels of inflammatory mediators and radical oxygen species were determined.
  
  
  RESULTS
  Treatment with telmisartan preserved endothelial NOS expression and inhibited inducible NOS and excessive NO generation, while reducing oxidation/nitration stress and inflammatory responses. Administration of telmisartan before CIH significantly ameliorated the CIH-induced myocardial apoptosis.
  
  
  CONCLUSIONS
  This study show that pre-CIH telmisartan administration ameliorated myocardial injury following CIH by attenuating CIH-induced myocardial apoptosis via regulation of NOS activity and inhibition of excessive NO generation, oxidation/nitration stress, and inflammatory responses.
authors.affiliation: Department of Respiratory and Critical Care Medicine, Tongji Hospital, Huazhong University of Science and Technology, No. 1095 Jiefang Road, Wuhan, 430030, China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Yuan
authors.forename: Die
authors.initials: D
authors.lastname: Zhu
authors.forename: Xue-ling
authors.initials: XL
authors.lastname: Guo
authors.forename: Yan
authors.initials: Y
authors.lastname: Deng
authors.forename: Jin
authors.initials: J
authors.lastname: Shang
authors.forename: Kui
authors.initials: K
authors.lastname: Liu
authors.forename: Hui-guo
authors.initials: HG
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001562:Benzimidazoles / Q000494:pharmacology*; D001565:Benzoates / Q000494:pharmacology*; D002097:C-Reactive Protein / Q000378:metabolism; D004195:Disease Models, Animal; D000860:Hypoxia / Q000473:pathology*; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009206:Myocardium / Q000166:cytology*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species; D020181:Sleep Apnea, Obstructive / Q000473:pathology*; D000077333:Telmisartan
chemical_list: D001562:Benzimidazoles; D001565:Benzoates; D018836:Inflammation Mediators; D015850:Interleukin-6; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D002097:C-Reactive Protein; D019001:Nitric Oxide Synthase; D000077333:Telmisartan