Determination of the rate of K+ movement through potassium channels in isolated rat heart and liver mitochondria

Biochimica et Biophysica Acta - Bioenergetics

Volumn 1777, Issue 6, 2008, Pages 540-548

  Bednarczyk, Piotr ^b,c   Barker, George D ^a   Halestrap, Andrew P ^a  

^a Dept Anat Sch Med Sci U   (United Kingdom)

^b UNIVERSITY OF WARSAW   (Poland)

^c NENCKI INSTITUTE OF EXPERIMENTAL BIOLOGY   (Poland)

Author keywords

Ischaemic preconditioning; Mitochondria; Mitochondrial ATP regulated potassium channel; Mitochondrial large conductance calcium activated potassium channel; Mitochondrial volume

Indexed keywords

LARGE CONDUCTANCE CALCIUM ACTIVATED POTASSIUM CHANNEL; NIGERICIN; PAXILLINE; POTASSIUM CHANNEL; VALINOMYCIN;

ANIMAL CELL; ARTICLE; CELL RESPIRATION; CONTROLLED STUDY; HEART MITOCHONDRION; LIGHT SCATTERING; LIVER MITOCHONDRION; MALE; NONHUMAN; POTASSIUM TRANSPORT; PREDICTION; PRIORITY JOURNAL; RAT;

ANIMALS; CATIONS, MONOVALENT; DOSE-RESPONSE RELATIONSHIP, DRUG; ION TRANSPORT; IONOPHORES; ISCHEMIC PRECONDITIONING, MYOCARDIAL; LARGE-CONDUCTANCE CALCIUM-ACTIVATED POTASSIUM CHANNEL ALPHA SUBUNITS; MALE; MITOCHONDRIA, HEART; MITOCHONDRIA, LIVER; MITOCHONDRIAL PROTEINS; NIGERICIN; OXYGEN CONSUMPTION; POTASSIUM; POTASSIUM CHANNELS; RATS; RATS, WISTAR; VALINOMYCIN;

RATTUS;

EID: 44649193822     PISSN: 00052728     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.bbabio.2008.04.018     Document Type: Article

References (53)

1. Halestrap A.P. The regulation of the matrix volume of mammalian mitochondria in vivo and in vitro, and its role in the control of mitochondrial metabolism. Biochim. Biophys. Acta 973 (1989) 355-382
2. + uniports and exchangers. J. Bioenerg. Biomembr. 26 (1994) 519-526
3. Bernardi P. Mitochondrial transport of cations: channels, exchangers, and permeability transition. Physiol. Rev. 79 (1999) 1127-1155
4. Hanley P.J., and Daut J. K-ATP channels and preconditioning: a re-examination of the role of mitochondrial K-ATP channels and an overview of alternative mechanisms. J. Mol. Cell. Cardiol. 39 (2005) 17-50
5. + cycle. Biochim. Biophys. Acta 1606 (2003) 23-41
6. Szewczyk A., Skalska J., Glab M., Kulawiak B., Malinska D., Koszela-Piotrowska I., and Kunz W.S. Mitochondrial potassium channels: from pharmacology to function. Biochim. Biophys. Acta 1757 (2006) 715-720
7. Hanley P.J., Mickel M., Loffler M., Brandt U., and Daut J. K-ATP channel-independent targets of diazoxide and 5-hydroxydecanoate in the heart. J. Physiol. 542 (2002) 735-741
8. Lim K.H.H., Javadov S.A., Das M., Clarke S.J., Suleiman M.S., and Halestrap A.P. The effects of ischaemic preconditioning, diazoxide and 5-hydroxydecanoate on rat heart mitochondrial volume and respiration. J. Physiol. 545 (2002) 961-974
9. Das M., Parker J.E., and Halestrap A.P. Matrix volume measurements challenge the existence of diazoxide/glibencamide-sensitive K-ATP channels in rat mitochondria. J. Physiol. 547 (2003) 893-902
10. Brustovetsky T., Shalbuyeva N., and Brustovetsky N. Lack of manifestations of diazoxide/5-hydroxydecanoatesensitive K-ATP channel in rat brain nonsynaptosomal mitochondria. J. Physiol. 568 (2005) 47-59
11. Grover G.J., and Garlid K.D. ATP-sensitive potassium channels: a review of their cardioprotective pharmacology. J. Mol. Cell. Cardiol. 32 (2000) 677-695
12. + channel in cardiac function and cardioprotection. Biochim. Biophys. Acta 1606 (2003) 1-21
13. Oldenburg O., Cohen M.V., and Downey J.M. Mitochondrial K-ATP channels in preconditioning. J. Mol. Cell. Cardiol. 35 (2003) 569-575
14. + channels and their role in cardioprotection. Circ. Res. 94 (2004) 420-432
15. Jung D.W., and Brierley G.P. The permeability of uncoupled heart mitochondria to potassium ion. J. Biol. Chem. 259 (1984) 6904-6911
16. + from heart mitochondria and the oxidation-reduction state of pyridine nucleotides. J. Biol. Chem. 256 (1981) 10490-10496
17. + ions. Arch. Biochem. Biophys. 199 (1980) 420-426
18. 2+ and regulates the intramitochondrial volume and adenine nucleotide content. Biochem. J. 246 (1987) 715-723
19. 2+], and its role in the hormonal regulation of mitochondrial matrix volume. Biochem. J. 258 (1989) 817-821
20. Davidson A.M., and Halestrap A.P. Inorganic pyrophosphate is located primarily in the mitochondria of the hepatocyte and increases in parallel with the decrease in light-scattering induced by gluconeogenic hormones, butyrate and ionophore A23187. Biochem. J. 254 (1988) 379-384
21. Quinlan P.T., Thomas A.P., Armston A.E., and Halestrap A.P. Measurement of the intramitochondrial volume in hepatocytes without cell disruption and its elevation by hormones and valinomycin. Biochem. J. 214 (1983) 395-404
22. + channels in the cardiac inner mitochondrial membrane. Science 298 (2002) 1029-1033
23. O'Rourke B., Cortassa S., and Aon M.A. Mitochondrial ion channels: gatekeepers of life and death. Physiology 20 (2005) 303-315
24. + channel opening requires superoxide radical generation. Am. J. Physiol. 290 (2006) H434-H440
25. Halestrap A.P., Clarke S.J., and Khaliulin I. The role of mitochondria in protection of the heart by preconditioning. Biochim. Biophys. Acta 1767 (2007) 1007-1031
26. Hughes W.A., and Halestrap A.P. The regulation of branched-chain 2-oxoacid dehydrogenase of liver, kidney and heart by phosphorylation. Biochem. J. 196 (1981) 459-469
27. Gornall A.G., Bardawill C.J., and David M.M. Determination of serum proteins by means of the biuret reaction. J. Biol. Chem. 177 (1949) 751-756
28. Halestrap A.P., and Dunlop J.L. Intramitochondrial regulation of fatty acid β-oxidation occurs between flavoprotein and ubiquinone. A role for changes in matrix volume. Biochem. J. 239 (1986) 559-565
29. 2+. Biochem. J. 244 (1987) 159-164
30. Nicholls D.G. Mitochondrial membrane potential and aging. Aging Cell 3 1 (2004) 35-40
31. + influx increases respiration and enhances ROS production while maintaining membrane potential. Am. J. Physiol. 292 (2007) C148-C156
32. Heinen A., Winning A., Schlack W., Hollmann M.W., Preckel B., Frabetadorf J., and Weber N.C. The regulation of mitochondrial respiration by opening of mK(Ca) channels is age-dependent. Eur. J. Pharmacol. 578 (2008) 108-113
33. Kopustinskiene D.M., Jovaisiene J., Liobikas J., and Toleikis A. Diazoxide and pinacidil uncouple pyruvate-malate-induced mitochondrial respiration. J. Bioenerg. Biomembr. 34 (2002) 49-53
34. Kopustinskiene D.M., Toleikis A., and Saris N.E.L. Adenine nucleotide translocase mediates the K-ATP-channel-openers-induced proton and potassium flux to the mitochondrial matrix. J. Bioenerg. Biomembr. 35 (2003) 141-148
35. Garlid K.D. Opening mitochondrial K-ATP in the heart - what happens, and what does not happen. Basic Res. Cardiol. 95 (2000) 275-279
36. + channel of heart mitochondria. Am. J. Physiol. 280 (2001) H649-H657
37. Lawrence C.L., Billups B., Rodrigo G.C., and Standen N.B. The K-ATP channel opener diazoxide protects cardiac myocytes during metabolic inhibition without causing mitochondrial depolarization or flavoprotein oxidation. Br. J. Pharmacol. 134 (2001) 535-542
38. Carroll R., Gant V.A., and Yellon D.M. Mitochondrial K-ATP channel opening protects a human atrial-derived cell line by a mechanism involving free radical generation. Cardiovasc. Res. 51 (2001) 691-700
39. Minners J., Lacerda L., Yellon D.M., Opie L.H., McLeod C.J., and Sack M.N. Diazoxide-induced respiratory inhibition - a putative mitochondrial K(ATP) channel independent mechanism of pharmacological preconditioning. Mol. Cell. Biochem. 294 (2007) 11-18
40. Holmuhamedov E.L., Jahangir A., Oberlin A., Komarov A., Colombini M., and Terzic A. Potassium channel openers are uncoupling protonophores: implication in cardioprotection. FEBS Lett. 568 (2004) 167-170
41. Schafer G., Portenhauser R., and Trolp R. Inhibition of mitochondrial metabolism by the diabetogenic thiadiazine diazoxide. I. Action on succinate dehydrogenase and TCA-cycle oxidations. Biochem. Pharmacol. 20 (1971) 1271-1280
42. Grimmsman T., and Rustenbeck I. Direct effects of diazoxide on mitochondria in pancreatic B-cells and on isolated liver mitochondria. Br. J. Pharmacol. 123 (1998) 781-788
43. Brennan J.P., Berry R.G., Baghai M., Duchen M.R., and Shattock M.J. FCCP is cardioprotective at concentrations that cause mitochondrial oxidation without detectable depolarisation. Cardiovasc. Res. 72 (2006) 322-330
44. Brennan J.P., Southworth R., Medina R.A., Davidson S.M., Duchen M.R., and Shattock M.J. Mitochondrial uncoupling, with low concentration FCCP, induces ROS-dependent cardioprotection independent of KATP channel activation. Cardiovasc. Res. 72 (2006) 313-321
45. Kabir A.M., Cao X., Gorog D.A., Tanno M., Bassi R., Bellahcene M., Quinlan R.A., Davis R.J., Flavell R.A., Shattock M.J., and Marber M.S. Antimycin A induced cardioprotection is dependent on pre-ischemic p38-MAPK activation but independent of MKK3. J. Mol. Cell. Cardiol. 39 (2005) 709-717
46. Chen Q., Camara A.K., Stowe D.F., Hoppel C.L., and Lesnefsky E.J. Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion. Am. J. Physiol. 292 (2007) C137-C147
47. Chen Q., Hoppel C.L., and Lesnefsky E.J. Blockade of electron transport before cardiac ischemia with the reversible inhibitor amobarbital protects rat heart mitochondria. J. Pharmacol. Exp. Ther. 316 (2006) 200-207
48. Lesnefsky E.J., Chen Q., Moghaddas S., Hassan M.O., Tandler B., and Hoppel C.L. Blockade of electron transport during ischemia protects cardiac mitochondria. J. Biol. Chem. 279 (2004) 47961-47967
49. Ockaili R.A., Bhargava P., and Kukreja R.C. Chemical preconditioning with 3-nitropropionic acid in hearts: role of mitochondrial K-ATP channel. Am. J. Physiol. 280 (2001) H2406-H2411
50. Kabir A.M., Clark J.E., Tanno M., Cao X., Hothersall J.S., Dashnyam S., Gorog D.A., Bellahcene M., Shattock M.J., and Marber M.S. Cardioprotection initiated by reactive oxygen species is dependent on activation of PKCepsilon. Am. J. Physiol. 291 (2006) H1893-H1899
51. Yellon D.M., and Downey J.M. Preconditioning the myocardium: From cellular physiology to clinical cardiology. Physiol. Rev. 83 (2003) 1113-1151
52. Forbes R.A., Steenbergen C., and Murphy E. Diazoxide-induced cardioprotection requires signaling through a redox-sensitive mechanism. Circ. Res. 88 (2001) 802-809
53. Khaliulin I., Schwalb H., Wang P., Houminer E., Grinberg L., Katzeff H., Borman J.B., and Powell S.R. Preconditioning improves postischemic mitochondrial function and diminishes oxidation of mitochondrial proteins. Free Radic. Biol. Med. 37 (2004) 1-9