Celiprolol, a selective β1-blocker, reduces the infarct size through production of nitric oxide in a rabbit model of myocardial infarction

Circulation Journal

Volumn 71, Issue 4, 2007, Pages 574-579

  Chen, Xuehai ^a   Minatoguchi, Shinya ^a   Arai, Masazumi ^a   Wang, Ningyuan ^a   Lu, Cuanjiang ^a   Narentuoya, Bao ^a   Uno, Yoshihiro ^a   Misao, Yu ^a   Takemura, Genzou ^a   Fujiwara, Takako ^b   Fujiwara, Hisayoshi ^a  

^a GIFU UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^b KYOTO WOMEN'S UNIVERSITY   (Japan)

Author keywords

Celiprolol; Infarct size; Mitochondrial KATP channel; Myocardial infarction; Nitric oxide

Indexed keywords

5 HYDROXYDECANOIC ACID; CELIPROLOL; EVANS BLUE; HYDROETHIDINE; N(G) NITROARGININE METHYL ESTER; NITRIC OXIDE; SUPEROXIDE; TRIPHENYLTETRAZOLIUM; BETA ADRENERGIC RECEPTOR BLOCKING AGENT; POTASSIUM CHANNEL;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; DOSE RESPONSE; DRUG ANTAGONISM; DRUG MECHANISM; HEART HEMODYNAMICS; HEART INFARCTION; HEART INFARCTION SIZE; HEART LEFT VENTRICLE; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; MALE; NONHUMAN; RABBIT; STAINING; ANIMAL; BLOOD PRESSURE; DISEASE MODEL; HEART MITOCHONDRION; HEART MUSCLE; HEART RATE; METABOLISM; PATHOLOGY; PHYSIOLOGY;

ADRENERGIC BETA-ANTAGONISTS; ANIMALS; BLOOD PRESSURE; CELIPROLOL; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; HEART RATE; MALE; MITOCHONDRIA, HEART; MYOCARDIAL INFARCTION; MYOCARDIUM; NITRIC OXIDE; POTASSIUM CHANNELS; RABBITS; SUPEROXIDES;

EID: 34047166363     PISSN: 13469843     EISSN: 13474820     Source Type: Journal    
DOI: 10.1253/circj.71.574     Document Type: Article

References (21)

1. Tolvanen JP, Wu X, Kahonen M, Sallinen K, Makynen H, Pekki A, et al. Effect of celiprolol therapy on arterial dilatation in experimental hypertension. Br J Pharmacol 1996; 119: 1137-1144.
2. Mori T, Hayashi T, Sohmiya K, Okuda N, Shimomura H, Ohkita M, et al. Mechanisms of combined treatment with celiprololo and candesartan for ventricular remodeling in experimental heart failure. Circ J 2005; 69: 596-602.
3. Asanuma H, Node K, Minamino T, Sanada S, Takashima S, Ueda Y, et al. Celiprolol increases coronary blood flow and reduces severity of myocardial ischemia via nitric oxide release. J Cardiovasc Pharmacol 2003; 41: 499-505.
4. Lebuffe G, Schumacker PT, Shao ZH, Anderson T, Iwase H, Vanden Hoek TL. ROS and NO trigger early preconditioning: Relationship to mitochondrial KATP channel. Am J Physiol Heart Circ Physiol 2003; 284: H299-H308.
5. Cuong DV, Kim N, Youm JB, Joo H, Warda M, Lee JW, et al. Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K channels in rat hearts. Am J Physiol Heart Circ Physiol 2006; 290: H1808-H1817.
6. Cin Q, Yang XM, Cui L, Critz SD, Cohen MV, Browner NC, et al. Exogenous NO triggers preconditioning via a cGMP- and mitoKATP-dependent mechanism. Am J Physiol Heart Circ Physiol 2004; 287: H712-H718.
7. Wang N, Minatoguchi S, Chen XH, Arai M, Uno Y, Lu Y, et al. Benidipine reduces myocardial infarct size involving reduction of hydroxyl radicals and production of protein kinase C-dependent nitric oxide in rabbits. J Cardiovasc Pharmacol 2004; 43: 747-757.
8. Miller FJ Jr, Gutterman DD, Rios C, Heistad DD, Davidson B. Superoxide production in vascular smooth muscle contributes to oxidative stress and impaired relaxation in atherosclerosis. Circ Res 1993; 72: 403-412.
9. Gross GJ, Peart JN. KATP channels and myocardial preconditioning: An update. Am J Physiol Heart Circ Physiol 2003; 285: H921-H930.
10. ATP channel openers on chronic left ventricular remodeling in the ischemic-reperfused rat heart. Circ J 2002, 66: 411-415.
11. ATP channels. Circ J 2002; 66: 763-768.
12. Shimizu Y, Minatoguchi S, Hashimoto K, Uno Y, Arai M, Wang N, et al. The role of serotonin in ischemic cellular damage and the infarct size reducing effect of sarpogrelate, a 5-HT2 receptor blocker, in rabbit hearts. J Am Coll Cardiol 2002; 40: 1347-1355.
13. Chen X, Minatoguchi S, Wang N, Arai M, Lu C, Uno Y, et al. Quinaprilt reduces myocardial infarct size involving nitric oxide production and mitochondrial KATP channel in rabbits. J Cardiovasc Pharmacol 2003; 41: 938-945.
14. Cohen RA, Weisbrod RM, Gericke M, Yaghoubi M, Bierl C, Bolotina VM. Mechanism of nitric oxide-induced vasodilatation: Refilling of intracellular stores by sarcoplasmic reticulum Ca2+ ATPase and inhibition of store operated Ca2+ influx. Circ Res 1999; 84: 210-219.
15. Tsao PS, McEvoy LM, Drexler H, Butcher EC, Cooke JP. Enhanced endothelial adhesiveness in hypercholesterolemia is attenuated by L-arginine. Circulation 1994; 89: 2176-2182.
16. Furlong B, Henderson AH, Lewis MJ, Smith JA. Endothelium-derived relaxing factor inhibits in vitro platelet aggregation. Br J Pharmacol 1987; 90: 687-692.
17. Yan ZQ, Yokota T, Zhang W, Hansson GK. Expression of inducible nitric oxide synthase inhibits platelet adhesion and restores blood flow in the injured artery. Circ Res 1996; 79: 38-44.
18. Kobayashi N, Mita S, Yoshida K, Honda T, Kobayashi T, Hara K, et al. Celiprolol activates eNOS through the PI3K-Akt pathway and inhibits VCAM-1 via NF-κB induced by oxidative stress. Hypertension 2003; 42: 1004-1013.
19. Bolli R. Oxygen-derived free radicals and postischemic myocardial dysfunctiojn ("stunned myocardium"). J Am Coll Cardiol 1988; 12: 239-249.
20. Kametani R, Miura T, Harada N, Shibuya M, Wang R, Tan H, et al. Carvedilol inhibits mitochondrial oxygen consumption and superoxide production during calcium overload in isolated heart mitochondria. Circ J 2006; 70: 321-326.
21. Inoue M, Sato E, Park AM, Nishikawa M, Kasahara E, Miyoshi M, et al. Cross-talk between NO and oxyradicals, a supersystem that regulates energy metabolism and survival of animals. Free Rad Res 2000; 33: 757-770.