Mitochondrial ATP-sensitive potassium channel opening inhibits isoproterenol-induced cardiac hypertrophy by preventing oxidative damage

Journal of Cardiovascular Pharmacology

Volumn 65, Issue 4, 2015, Pages 393-397

  Caldas, Francisco Rodrigo Lemos ^a   Leite, Iago Mateus Rocha ^a   Filgueiras, Ana Beatriz Tavarez ^a   De Figueiredo, Isaias Lima ^a   De Sousa, Tereza Amália Gomes Marques ^a   Martins, Pamela Reis ^a   Kowaltowski, Alicia Juliana ^b   Facundo, Heberty Di Tarso Fernandes ^a  

^a Aldeota   (Brazil)

^b UNIVERSITY OF SÃO PAULO   (Brazil)

Author keywords

Antioxidants; Cardiac hypertrophy; Diazoxide; Mitochondria; Oxidative stress

Indexed keywords

5 HYDROXYDECANOIC ACID; ADENOSINE TRIPHOSPHATE SENSITIVE POTASSIUM CHANNEL; CATALASE; DIAZOXIDE; GLIBENCLAMIDE; GLUTATHIONE; PROTEIN; REACTIVE OXYGEN METABOLITE; SUPEROXIDE DISMUTASE; THIOL; ANTIOXIDANT; CARDIOTONIC AGENT; MITOCHONDRIAL K(ATP) CHANNEL; POTASSIUM CHANNEL; VASODILATOR AGENT;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BODY WEIGHT; BONE LENGTH; CONTROLLED STUDY; ENZYME ACTIVITY; HEART INJURY; HEART PROTECTION; HEART WEIGHT; ISOPROTERENOL-INDUCED CARDIAC HYPERTROPHY; MALE; MITOCHONDRION; MOUSE; NONHUMAN; OXIDATION REDUCTION STATE; OXIDATIVE STRESS; PRIORITY JOURNAL; TIBIA; ANIMAL; CARDIOMEGALY; DISEASE MODEL; DRUG EFFECTS; HEART MITOCHONDRION; METABOLISM; TREATMENT OUTCOME;

ANIMALS; ANTIOXIDANTS; CARDIOMEGALY; CARDIOTONIC AGENTS; DIAZOXIDE; DISEASE MODELS, ANIMAL; MICE; MITOCHONDRIA, HEART; OXIDATIVE STRESS; POTASSIUM CHANNELS; TREATMENT OUTCOME; VASODILATOR AGENTS;

EID: 84928167359     PISSN: 01602446     EISSN: 15334023     Source Type: Journal    
DOI: 10.1097/FJC.0000000000000210     Document Type: Article

References (27)

1. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics - 2013 update: a report from the American Heart Association. Circulation. 2013;127:e6-e245.
2. Frey N, McKinsey TA, Olson EN. Decoding calcium signals involved in cardiac growth and function. Nat Med. 2000;6:1221-1227.
3. Osterholt M, Nguyen TD, Schwarzer M, et al. Alterations in mitochondrial function in cardiac hypertrophy and heart failure. Heart Fail Rev. 2013;18:645-656.
4. Date M, Morita T, Yamashita N, et al. The antioxidant N-2-mercaptopropionyl glycine attenuates left ventricular hypertrophy in in vivo murine pressure-overload model. J Am Coll Cardiol. 2002;39:907-912.
5. Dhalla AK, Hill MF, Singal PK. Role of oxidative stress in transition of hypertrophy to heart failure. J Am Coll Cardiol. 1996;28:506-514.
6. Hirotani S, Otsu K, Nishida K, et al. Involvement of nuclear factor-kappaB and apoptosis signal-regulating kinase 1 in G-protein-coupled receptor agonist-induced cardiomyocyte hypertrophy. Circulation. 2002;105:509-515.
7. Pimentel DR, Amin JK, Xiao L, et al. Reactive oxygen species mediate amplitude-dependent hypertrophic and apoptotic responses to mechanical stretch in cardiac myocytes. Circ Res. 2001;89:453-460.
8. Dai D-F, Santana LF, Vermulst M, et al. Overexpression of catalase targeted to mitochondria attenuates murine cardiac aging. Circulation. 2009;119:2789-2797.
9. Kwon SH, Pimentel DR, Remondino A, et al. H(2)O(2) regulates cardiac myocyte phenotype via concentration-dependent activation of distinct kinase pathways. J Mol Cell Cardiol. 2003;35:615-621.
10. Siwik DA, Tzortzis JD, Pimental DR, et al. Inhibition of copper-zinc superoxide dismutase induces cell growth, hypertrophic phenotype, and apoptosis in neonatal rat cardiac myocytes in vitro. Circ Res. 1999;85: 147-153.
11. Madamanchi NR, Runge MS. Redox signaling in cardiovascular health and disease. Free Radic Biol Med. 2013;61:473-501.
12. Griffiths ER, Friehs I, Scherr E, et al. Electron transport chain dysfunction in neonatal pressure-overload hypertrophy precedes cardiomyocyte apoptosis independent of oxidative stress. J Thorac Cardiovasc Surg. 2010;139:1609-1617.
13. Koyama H, Nojiri H, Kawakami S, et al. Antioxidants improve the phenotypes of dilated cardiomyopathy and muscle fatigue in mitochondrial superoxide dismutase-deficient mice. Molecules. 2013;18:1383-1393.
14. Kuroda J, Ago T, Matsushima S, et al. NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart. Proc Natl Acad Sci U S A. 2010;107:15565-15570.
15. Facundo HTF, Carreira RS, de Paula JG, et al. Ischemic preconditioning requires increases in reactive oxygen release independent of mitochondrial K+ channel activity. Free Radic Biol Med. 2006;40:469-479.
16. Facundo HTF, de Paula JG, Kowaltowski AJ. Mitochondrial ATPsensitive K+ channels prevent oxidative stress, permeability transition and cell death. J Bioenerg Biomembr. 2005;37:75-82.
17. Akopova OV, Kolchinskaya LI, Nosar VI, et al. Effect of potential-dependent potassium uptake on production of reactive oxygen species in rat brain mitochondria. Biochemistry (Mosc). 2014;79:44-53.
18. Morota S, Piel S, Hansson MJ. Respiratory uncoupling by increased H(+) or K(+) flux is beneficial for heart mitochondrial turnover of reactive oxygen species but not for permeability transition. BMC Cell Biol. 2013;14:40.
19. Vanden Hoek T, Becker LB, Shao ZH, et al. Preconditioning in cardiomyocytes protects by attenuating oxidant stress at reperfusion. Circ Res. 2000;86:541-548.
20. O'Rourke B. Evidence for mitochondrial K+ channels and their role in cardioprotection. Circ Res. 2004;94:420-432.
21. Yonemochi H, Ichinose M, Anan F, et al. Diazoxide-induced cardioprotection via DeltaPsim loss depending on timing of application. Life Sci. 2006;79:1906-1912.
22. Alberici LC, Paim BA, Zecchin KG, et al. Activation of the mitochondrial ATP-sensitive K+ channel reduces apoptosis of spleen mononuclear cells induced by hyperlipidemia. Lipids Health Dis. 2013;12:87.
23. De Windt LJ, Lim HW, Bueno OF, et al. Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo. Proc Natl Acad Sci U S A. 2001;98:3322-3327.
24. Xia Y, Rajapurohitam V, Cook MA, et al. Inhibition of phenylephrine induced hypertrophy in rat neonatal cardiomyocytes by the mitochondrial KATP channel opener diazoxide. J Mol Cell Cardiol. 2004;37:1063-1067.
25. Coetzee WA. Multiplicity of effectors of the cardioprotective agent, diazoxide. Pharmacol Ther. 2013;140:167-175.
26. Shih NL, Cheng TH, Loh SH, et al. Reactive oxygen species modulate angiotensin II-induced beta-myosin heavy chain gene expression via Ras/Raf/extracellular signal-regulated kinase pathway in neonatal rat cardiomyocytes. Biochem Biophys Res Commun. 2001;283:143-148.
27. González G, Zaldívar D, Carrillo E, et al. Pharmacological preconditioning by diazoxide downregulates cardiac L-type Ca(2+) channels. Br J Pharmacol. 2010;161:1172-1185.