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From the Department of Medicine, Montreal Heart Institute (G.-R.L., J.F., S.N.) and University of Montreal (G.-R.L., S.N.), the Department of Surgery, Montreal Heart Institute and University of Montreal (M.C.), and the Department of Pharmacology and Therapeutics, McGill University (L.Y., S.N.), Montreal, Canada.
Correspondence to Dr Stanley Nattel, Research Center, Montreal Heart Institute, 5000 Belanger St E, Montreal, Quebec, Canada H1T 1C8.
Abstract Previous voltage-clamp studies have suggested that the delayed rectifier current (IK) is small or absent in the human ventricle and, when present, consists only of the rapid component (IKr); however, molecular studies suggest the presence of functionally important IK in the human heart, specific IKr blockers are known to delay ventricular repolarization and cause the long QT syndrome in humans, and we have shown that the expression of IK is strongly influenced by cell isolation techniques. The present experiments were designed to assess the expression of IK in myocytes obtained by arterial perfusion of right ventricular tissue from explanted human hearts. Of 35 cells from three hearts, 33 (94%) showed time-dependent currents typical of IK. The envelope-of-tails test was not satisfied under control conditions but became satisfied in the presence of the benzenesulfonamide E-4031 (5 µmol/L). E-4031 suppressed a portion of IK in 32 of 33 cells, with properties of the drug-sensitive and -resistant components consistent with previous descriptions of IKr and the slow component (IKs), respectively. Action potential duration to 95% repolarization at 1 Hz was prolonged by E-4031 from 336±16 (mean±SEM) to 421±19 ms (n=5, P<.01), indicating a functional role for IK. Indapamide, a diuretic agent previously shown to inhibit IKs selectively, suppressed E-4031resistant current. The presence of a third type of delayed rectifier, the ultrarapid delayed rectifier current (IKur), was evaluated with the use of depolarizing prepulses and low concentrations (50 µmol/L) of 4-aminopyridine. Although these techniques revealed clear IKur in five of five human atrial cells, no corresponding component was observed in any of five human ventricular myocytes. We conclude that a functionally significant IK, with components corresponding to IKr and IKs, is present in human ventricular cells, whereas IKur appears to be absent. These findings are important for understanding the molecular, physiological, and pharmacological determinants of human ventricular repolarization and arrhythmias.
Key Words: repolarization cardiac arrhythmias ion channels antiarrhythmic agents class III drugs
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P. G. A. Volders, K. R. Sipido, E. Carmeliet, R. L. H. M. G. Spatjens, H. J. J. Wellens, and M. A. Vos Repolarizing K+ Currents ITO1 and IKs Are Larger in Right Than Left Canine Ventricular Midmyocardium Circulation, January 19, 1999; 99(2): 206 - 210. [Abstract] [Full Text] [PDF] |
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P. Geelen, B. Drolet, E. Lessard, P. Gilbert, G. E. O'Hara, and J. Turgeon Concomitant Block of the Rapid (IKr) and Slow (IKs) Components of the Delayed Rectifier Potassium Current is Associated With Additional Drug Effects on Lengthening of Cardiac Repolarization Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 1999; 4(3): 143 - 150. [Abstract] [PDF] |
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G.-R. Li, B. Yang, J. Feng, R. F. Bosch, M. Carrier, and S. Nattel Transmembrane ICa contributes to rate-dependent changes of action potentials in human ventricular myocytes Am J Physiol Heart Circ Physiol, January 1, 1999; 276(1): H98 - H106. [Abstract] [Full Text] [PDF] |
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X.-K. Liu, A. Katchman, S. N. Ebert, and R. L. Woosley The Antiestrogen Tamoxifen Blocks the Delayed Rectifier Potassium Current, IKr, in Rabbit Ventricular Myocytes J. Pharmacol. Exp. Ther., December 1, 1998; 287(3): 877 - 883. [Abstract] [Full Text] |
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N. Iost, L. Virag, M. Opincariu, J. Szecsi, Andras Varro, and J. Gy. Papp Delayed rectifier potassium current in undiseased human ventricular myocytes Cardiovasc Res, December 1, 1998; 40(3): 508 - 515. [Abstract] [Full Text] [PDF] |
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J. Feng, D. Xu, Z. Wang, and S. Nattel Ultrarapid delayed rectifier current inactivation in human atrial myocytes: properties and consequences Am J Physiol Heart Circ Physiol, November 1, 1998; 275(5): H1717 - H1725. [Abstract] [Full Text] [PDF] |
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S. Kupershmidt, D. J. Snyders, A. Raes, and D. M. Roden A K+ Channel Splice Variant Common in Human Heart Lacks a C-terminal Domain Required for Expression of Rapidly Activating Delayed Rectifier Current J. Biol. Chem., October 16, 1998; 273(42): 27231 - 27235. [Abstract] [Full Text] [PDF] |
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S. Kaab, J. Dixon, J. Duc, D. Ashen, M. Nabauer, D. J. Beuckelmann, G. Steinbeck, D. McKinnon, and G. F. Tomaselli Molecular Basis of Transient Outward Potassium Current Downregulation in Human Heart Failure : A Decrease in Kv4.3 mRNA Correlates With a Reduction in Current Density Circulation, October 6, 1998; 98(14): 1383 - 1393. [Abstract] [Full Text] [PDF] |
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C. Chouabe, M.-D. Drici, G. Romey, J. Barhanin, and M. Lazdunski HERG and KvLQT1/IsK, the Cardiac K+ Channels Involved in Long QT Syndromes, Are Targets for Calcium Channel Blockers Mol. Pharmacol., October 1, 1998; 54(4): 695 - 703. [Abstract] [Full Text] |
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P. Babij, G. R. Askew, B. Nieuwenhuijsen, C.-M. Su, T. R. Bridal, B. Jow, T. M. Argentieri, J. Kulik, L. J. DeGennaro, W. Spinelli, et al. Inhibition of Cardiac Delayed Rectifier K+ Current by Overexpression of the Long-QT Syndrome HERG G628S Mutation in Transgenic Mice Circ. Res., September 21, 1998; 83(6): 668 - 678. [Abstract] [Full Text] [PDF] |
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G.-R. Li, J. Feng, L. Yue, and M. Carrier Transmural heterogeneity of action potentials and Ito1 in myocytes isolated from the human right ventricle Am J Physiol Heart Circ Physiol, August 1, 1998; 275(2): H369 - H377. [Abstract] [Full Text] [PDF] |
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Y. Lu, L. Yue, Z. Wang, and S. Nattel Effects of the Diuretic Agent Indapamide on Na+, Transient Outward, and Delayed Rectifier Currents in Canine Atrial Myocytes Circ. Res., July 27, 1998; 83(2): 158 - 166. [Abstract] [Full Text] [PDF] |
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K. S. Lee and E. W. Lee Ionic Mechanism of Ibutilide in Human Atrium: Evidence for a Drug-Induced Na+ Current Through a Nifedipine Inhibited Inward Channel J. Pharmacol. Exp. Ther., July 1, 1998; 286(1): 9 - 22. [Abstract] [Full Text] |
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M. Tristani-Firouzi and M. C Sanguinetti Voltage-dependent inactivation of the human K+ channel KvLQT1 is eliminated by association with minimal K+ channel (minK) subunits J. Physiol., July 1, 1998; 510(1): 37 - 45. [Abstract] [Full Text] [PDF] |
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L. Priebe and D. J. Beuckelmann Simulation Study of Cellular Electric Properties in Heart Failure Circ. Res., June 15, 1998; 82(11): 1206 - 1223. [Abstract] [Full Text] [PDF] |
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B. London, D. W Wang, J. A Hill, and P. B Bennett The transient outward current in mice lacking the potassium channel gene Kv1.4 J. Physiol., May 15, 1998; 509(1): 171 - 182. [Abstract] [Full Text] [PDF] |
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X.-K. Liu, A. Katchman, M.-D. Drici, S. N. Ebert, I. Ducic, M. Morad, and R. L. Woosley Gender Difference in the Cycle Length-Dependent QT and Potassium Currents in Rabbits J. Pharmacol. Exp. Ther., May 1, 1998; 285(2): 672 - 679. [Abstract] [Full Text] |
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R. F. Bosch, R. Gaspo, A. E. Busch, H. J. Lang, G.-R. Li, and S. Nattel Effects of the chromanol 293B, a selective blocker of the slow, component of the delayed rectifier K+ current, on repolarization in human and guinea pig ventricular myocytes Cardiovasc Res, May 1, 1998; 38(2): 441 - 450. [Abstract] [Full Text] [PDF] |
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E. P. Baskin and J. J. Lynch Jr. Differential Atrial versus Ventricular Activities of Class III Potassium Channel Blockers J. Pharmacol. Exp. Ther., April 1, 1998; 285(1): 135 - 142. [Abstract] [Full Text] |
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S. Nattel Experimental evidence for proarrhythmic mechanisms of antiarrhythmic drugs Cardiovasc Res, March 1, 1998; 37(3): 567 - 577. [Abstract] [Full Text] [PDF] |
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B. Drolet, M. Khalifa, P. Daleau, B. A. Hamelin, and J. Turgeon Block of the Rapid Component of the Delayed Rectifier Potassium Current by the Prokinetic Agent Cisapride Underlies Drug-Related Lengthening of the QT Interval Circulation, January 20, 1998; 97(2): 204 - 210. [Abstract] [Full Text] [PDF] |
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B. London, M. C. Trudeau, K. P. Newton, A. K. Beyer, N. G. Copeland, D. J. Gilbert, N. A. J enkins, C. A. Satler, and G. A. Robertson Two Isoforms of the Mouse Ether-a-go-go–Related Gene Coassemble to Form Channels With Properties Similar to the Rapidly Activating Component of the Cardiac Delayed Rectifier K+ Current Circ. Res., November 19, 1997; 81(5): 870 - 878. [Abstract] [Full Text] |
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J. Toyama, K. Kamiya, J. Cheng, J.-K. Lee, R. Suzuki, and I. Kodama Vesnarinone Prolongs Action Potential Duration Without Reverse Frequency Dependence in Rabbit Ventricular Muscle by Blocking the Delayed Rectifier K+ Current Circulation, November 18, 1997; 96(10): 3696 - 3703. [Abstract] [Full Text] |
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C. Fiset, B. Drolet, B. A. Hamelin, and J. Turgeon Block of IKs by the Diuretic Agent Indapamide Modulates Cardiac Electrophysiological Effects of the Class III Antiarrhythmic Drug dl-Sotalol J. Pharmacol. Exp. Ther., October 1, 1997; 283(1): 148 - 156. [Abstract] [Full Text] |
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F. Y. Shalaby, P. C. Levesque, W.-P. Yang, W. A. Little, M. L. Conder, T. Jenkins-West, and M. A. Blanar Dominant-Negative KvLQT1 Mutations Underlie the LQT1 Form of Long QT Syndrome Circulation, September 16, 1997; 96(6): 1733 - 1736. [Abstract] [Full Text] |
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E. Delpon, C. Valenzuela, P. Gay, L. Franqueza, D. J Snyders, and J. Tamargo Block of human cardiac Kv1.5 channels by loratadine: voltage-, time- and use-dependent block at concentrations above therapeutic levels Cardiovasc Res, August 1, 1997; 35(2): 341 - 350. [Abstract] [Full Text] [PDF] |
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M. V. Brahmajothi, M. J. Morales, K. A. Reimer, and H. C. Strauss Regional Localization of ERG, the Channel Protein Responsible for the Rapid Component of the Delayed Rectifier, K+ Current in the Ferret Heart Circ. Res., July 19, 1997; 81(1): 128 - 135. [Abstract] [Full Text] |
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