Contribution of L-type Ca2+ channels to early afterdepolarizations induced by IKr and IKs channel suppression in guinea pig ventricular myocytes

Journal of Membrane Biology

Volumn 222, Issue 3, 2008, Pages 151-166

  Yamada, Mitsuhiko ^a   Ohta, Keisuke ^a   Niwa, Atsunori ^a   Tsujino, Natsuko ^a   Nakada, Tsutomu ^a   Hirose, Masamichi ^a  

^a SHINSHU UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

Action potential clamp; Cardiac electrophysiology; Early afterdepolarization; IKr channel; IKs channel; L type Ca2+ channel; Long QT syndrome

Indexed keywords

1 [2 (6 METHYL 2 PYRIDYL)ETHYL] 4 (4 METHYLSULFONYLAMINOBENZOYL)PIPERIDINE; 2 [4 (2,5 DIFLUOROBENZYLOXY)PHENOXY] 5 ETHOXYANILINE; CALCIUM CHANNEL L TYPE; CHROMANOL 293B; INWARDLY RECTIFYING POTASSIUM CHANNEL; INWARDLY RECTIFYING POTASSIUM CHANNEL IKR; INWARDLY RECTIFYING POTASSIUM CHANNEL IKS; NIFEDIPINE;

ACTION POTENTIAL; ANIMAL CELL; ANIMAL TISSUE; ARTICLE; CALCIUM CURRENT; CONTROLLED STUDY; DRUG EFFECT; GUINEA PIG; HEART DEPOLARIZATION; HEART MUSCLE CELL; HEART REPOLARIZATION; HEART VENTRICLE WALL; MALE; MEMBRANE DEPOLARIZATION; NONHUMAN; POTASSIUM CURRENT; PROTEIN FUNCTION;

ACTION POTENTIALS; ANIMALS; CALCIUM CHANNEL BLOCKERS; CALCIUM CHANNELS, L-TYPE; CELLS, CULTURED; GUINEA PIGS; HEART VENTRICLES; MALE; MYOCYTES, CARDIAC; NIFEDIPINE; POTASSIUM CHANNEL BLOCKERS; POTASSIUM CHANNELS, INWARDLY RECTIFYING; POTASSIUM CHANNELS, VOLTAGE-GATED;

CAVIA;

EID: 46149098871     PISSN: 00222631     EISSN: None     Source Type: Journal    
DOI: 10.1007/s00232-008-9113-9     Document Type: Article

References (42)

1. 2+ channel inactivation in controlling heart excitation. Proc Natl Acad Sci USA 99:17185-17190
2. ++/calmodulin-dependent protein kinase, decreases early afterdepolarizations in rabbit heart. J Pharmacol Exp Ther 287:996-1006
3. Antzelevitch C, Shimizu W (2002) Cellular mechanisms underlying the long QT syndrome. Curr Opin Cardiol 17:43-51
4. Armoundas AA, Hobai IA, Tomaselli GF, Winslow RL, O'Rourke B (2003) Role of sodium-calcium exchanger in modulating the action potential of ventricular myocytes from normal and failing hearts. Circ Res 93:46-53
5. 2+ transients under action potential clamp in guinea pig ventricular myocytes. Am J Physiol 261:C393-C397
6. 2+ current in canine ventricular cardiomyocytes. Naunyn-Schmiedebergs Arch Pharmacol 372:63-70
7. Blaustein MP, Lederer WJ (1999) Sodium/calcium exchange: its physiological implications. Physiol Rev 79:763-854
8. + current, on repolarization in human and guinea pig ventricular myocytes. Cardiovasc Res 38:441-450
9. Brugada P, Wellens HJJ (1985) Early afterdepolarizations: role in conduction block, "prolonged repolarization-dependent reexcitation," and tachyarrhythmia in the human heart. Pace 8:889-896
10. Cranefield PF, Aronson RS (1988) The causes, characteristics, and consequences of early afterdepolarizations. In: Cranefield PF, Aronson RS (eds) Cardiac arrhythmias: the role of triggered activity and other mechanisms. Futura, New York, pp 431-479
11. Daleau P, Khalifa M, Turgeon J (1997) Effects of cadmium and nisoldipine on the delayed rectifier potassium current in guinea pig ventricular myocytes. J Pharmacol Exp Ther 281:826-833
12. Damiano BP, Rose MR (1984) Effects of pacing on triggered activity induced by early afterdepolarizations. Circulation 5:1013-1025
13. Doerr T, Denger R, Doerr A, Trautwein W (1990) Ionic currents contributing to the action potential in single ventricular myocytes of the guinea pig studied with action potential clamp. Pfluegers Arch 416:230-237
14. Fabiato A (1985) Simulated calcium current can both cause calcium loading in and trigger calcium release from the sarcoplasmic reticulum of a skinned canine cardiac Purkinje cell. J Gen Physiol 85:291-320
15. 2+ channel currents in guinea pig ventricular myocytes. J Physiol 541:731-740
16. 2+ influx during the cardiac action potential in guinea pig ventricular myocytes. Circ Res 79:194-200
17. Hamill OP, Marty A, Neher E, Sakmann B, Sigworth FJ (1981) Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches. Pfluegers Arch 391:85-100
18. 2+ channels in guinea pig ventricular myocytes through independent mechanisms. J Physiol 444:257-268
19. Hoffman BB (2006) Therapy of hypertension. In: Brunton LL (ed) The pharmacological basis of therapeutics, 11th edn. McGraw-Hill, New York, pp 845-868
20. 2+ current. Circ Res 64:977-990
21. Kass RS, Sanguinetti MC (1984) Inactivation of calcium channel current in the calf cardiac Purkinje fiber. Evidence for voltage- and calcium-mediated mechanisms. J Gen Physiol 84:705-726
22. Keating MT, Sanguinetti MC (2001) Molecular and cellular mechanisms of cardiac arrhythmias. Cell 104:569-580
23. Lee KS, Marbán E, Tsien RW (1985) Inactivation of calcium channels in mammalian heart cells: joint dependence on membrane potential and intracellular calcium. J Physiol 364:395-411
24. Linz KW, Myer R (1998a) Control of L-type calcium current during the action potential of guinea pig ventricular myocytes. J Physiol 513:425-442
25. Linz KW, Myer R (1998b) The late component of L-type calcium current during guinea pig cardiac action potentials and its contribution to contraction. Pfluegers Arch 436:679-688
26. Linz KW, Myer R (2000) Profile and kinetics of L-type calcium current during the cardiac ventricular action potential compared in guinea pigs, rats and rabbits. Pfluegers Arch 439:588-599
27. Luo C-H, Rudy Y (1994) A dynamic model of the cardiac ventricular action potential. I Simulations of ionic currents and concentration changes. Circ Res 74:1071-1096
28. Marbán E, Robinson SW, Wier WG (1986) Mechanisms of arrhythmogenic delayed and early afterdepolarizations in ferret ventricular muscle. J Clin Invest 78:1185-1192
29. 2+ exchanger, attenuates reperfusion injury in the in vitro and in vivo cerebral ischemic models. J Pharmacol Exp Ther 298:249-256
30. McDonald TF, Pelzer S, Trautwein W, Pelzer DJ (1994) Regulation and modulation of calcium channels in cardiac, skeletal, and smooth muscle cells. Physiol Rev 74:365-507
31. Michel T (2006) Treatment of myocardial ischemia. In: Brunton LL (ed) The pharmacological basis of therapeutics, 11th edn. McGraw-Hill, New York, pp 823-844
32. Nagy ZA, Virág L, Tóth A, Biliczki P, Acsai K, Bányász T, Nánási P, Papp JG, Varró A (2004) Selective inhibition of sodium-calcium exchanger by SEA-0400 decreases early and delayed afterpolarization in canine heart. Br J Pharmacol 143:827-831
33. Priori SG, Corr PB (1990) Mechanisms underlying early and delayed afterpolarizations induced by catecholamines. Am J Physiol 27:H1796-H1805
34. + current. Differential sensitivity to block by class III antiarrhythmic agents. J Gen Physiol 96:195-215
35. Schwartz PJ (2005) Management of long QT syndrome. Nat Clin Pract Cardiovasc Med 2:346-351
36. Shimizu W, Ohe T, Kurita T, Kawade M, Arakaki Y, Aihara N, Kamakura S, Kamiya T, Shimomura K (1995) Effects of verapamil and propranolol on early afterdepolarizations and ventricular arrhythmias induced by epinephrine in congenital long QT syndrome. J Am Coll Cardiol 26:1299-1309
37. 2+ channels does not affect their voltage sensor. J Gen Physiol 102:1005-1030
38. Sicouri S, Quist M, Antzelevitch C (1996) Evidence for the presence of M cells in the guinea pig ventricle. J Cardiovasc Electrophysiol 7:503-511
39. v1.2 calcium channel dysfunction causes a multisystem disorder including arrhythmia and autism. Cell 119:19-31
40. 2+ current: a cellular mechanism for long Q-T arrhythmias. Am J Physiol 276:H2168-H2178
41. + channel through the same mechanism. J Biol Chem 268:24551-24554
42. Zeng J, Rudy Y (1995) Early afterdepolarizations in cardiac myocytes: mechanism and rate dependence. Biophys J 68:949-964