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In the experiments here, the time- and voltage-dependent properties of the Ca2+-independent, depolarization-activated K+ currents in adult mouse ventricular myocytes were characterized in detail. In the majority (65 of 72,
90%) of cells dispersed from the ventricles, analysis of the decay phases of the outward currents revealed three distinct K+ current components: a rapidly inactivating, transient outward K+ current, Ito,f (mean ± SEM 
decay = 85 ± 2 ms); a slowly (mean ± SEM decay = 1,162 ± 29 ms) inactivating K+ current, IK,slow; and a non inactivating, steady state current, Iss. In a small subset (7 of 72, 10%) of cells, Ito,f was absent and a slowly inactivating (mean ± SEM decay = 196 ± 7 ms) transient outward current, referred to as Ito,s, was identified; the densities and properties of IK,slow and Iss in Ito,s-expressing cells are indistinguishable from the corresponding currents in cells with Ito,f. Microdissection techniques were used to remove tissue pieces from the left ventricular apex and from the ventricular septum to allow the hypothesis that there are regional differences in Ito,f and Ito,s expression to be tested directly. Electrophysiological recordings revealed that all cells isolated from the apex express Ito,f (n = 35); Ito,s is not detected in these cells (n = 35). In the septum, by contrast, all of the cells express Ito,s (n = 28) and in the majority (22 of 28, 80%) of cells, Ito,f is also present. The density of Ito,f (mean ± SEM at +40 mV = 6.8 ± 0.5 pA/pF, n = 22) in septum cells, however, is significantly (P < 0.001) lower than Ito,f density in cells from the apex (mean ± SEM at +40 mV = 34.6 ± 2.6 pA/pF, n = 35). In addition to differences in inactivation kinetics, Ito,f, Ito,s, and IK,slow display distinct rates of recovery (from inactivation), as well as differential sensitivities to 4-aminopyridine (4-AP), tetraethylammonium (TEA), and Heteropoda toxin-3. IK,slow, for example, is blocked selectively by low (10–50 µM) concentrations of 4-AP and by (
25 mM) TEA. Although both Ito,f and Ito,s are blocked by high (>100 µM) 4-AP concentrations and are relatively insensitive to TEA, Ito,f is selectively blocked by nanomolar concentrations of Heteropoda toxin-3, and Ito,s (as well as IK,slow and Iss) is unaffected. Iss is partially blocked by high concentrations of 4-AP or TEA. The functional implications of the distinct properties and expression patterns of Ito,f and Ito,s, as well as the likely molecular correlates of these (and the IK,slow and Iss) currents, are discussed.
Key Words: Ito,f • Ito,s • transient outward currents • delayed rectifier • transgenic mice
Abbreviations: 4-AP, 4-aminopyridine; DTX, dendrotoxin; HpTx-3, Heteropoda toxin 3; TEA, tetraethylammonium
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J. M Nerbonne Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium J. Physiol., June 1, 2000; 525(2): 285 - 298. [Abstract] [Full Text] [PDF]
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W. H. DuBell, W. J. Lederer, and T. B. Rogers K+ currents responsible for repolarization in mouse ventricle and their modulation by FK-506 and rapamycin Am J Physiol Heart Circ Physiol, March 1, 2000; 278(3): H886 - H897. [Abstract] [Full Text] [PDF]
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W. Guo, H. Xu, B. London, and J. M Nerbonne Molecular basis of transient outward K+ current diversity in mouse ventricular myocytes J. Physiol., December 15, 1999; 521(3): 587 - 599. [Abstract] [Full Text] [PDF]
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H. Xu, D. M. Barry, H. Li, S. Brunet, W. Guo, and J. M. Nerbonne Attenuation of the Slow Component of Delayed Rectification, Action Potential Prolongation, and Triggered Activity in Mice Expressing a Dominant-Negative Kv2 {alpha} Subunit Circ. Res., October 1, 1999; 85(7): 623 - 633. [Abstract] [Full Text] [PDF]
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H. Xu, H. Li, and J. M Nerbonne Elimination of the transient outward current and action potential prolongation in mouse atrial myocytes expressing a dominant negative Kv4 {alpha} subunit J. Physiol., August 15, 1999; 519(1): 11 - 21. [Abstract] [Full Text] [PDF]
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E. Bou-Abboud and J. M Nerbonne Molecular correlates of the calcium-independent, depolarization-activated K+ currents in rat atrial myocytes J. Physiol., June 1, 1999; 517(2): 407 - 420. [Abstract] [Full Text] [PDF]
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M. Song, G. Helguera, M. Eghbali, N. Zhu, M. M. Zarei, R. Olcese, L. Toro, and E. Stefani Remodeling of Kv4.3 Potassium Channel Gene Expression under the Control of Sex Hormones J. Biol. Chem., August 17, 2001; 276(34): 31883 - 31890. [Abstract] [Full Text] [PDF]
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W. H. duBell, M. S. Gigena, S. Guatimosim, X. Long, W. J. Lederer, and T. B. Rogers Effects of PP1/PP2A inhibitor calyculin A on the E-C coupling cascade in murine ventricular myocytes Am J Physiol Heart Circ Physiol, January 1, 2002; 282(1): H38 - H48. [Abstract] [Full Text] [PDF]
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B. London, W. Guo, X.-h. Pan, J. S. Lee, V. Shusterman, C. J. Rocco, D. A. Logothetis, J. M. Nerbonne, and J. A. Hill Targeted Replacement of Kv1.5 in the Mouse Leads to Loss of the 4-Aminopyridine-Sensitive Component of IK,slow and Resistance to Drug-Induced QT Prolongation Circ. Res., May 11, 2001; 88(9): 940 - 946. [Abstract] [Full Text] [PDF]
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J. M.B. Anumonwo, Y. N. Tallini, F. J. Vetter, and J. Jalife Action Potential Characteristics and Arrhythmogenic Properties of the Cardiac Conduction System of the Murine Heart Circ. Res., August 17, 2001; 89(4): 329 - 335. [Abstract] [Full Text] [PDF]
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V. Trepanier-Boulay, C. St-Michel, A. Tremblay, and C. Fiset Gender-Based Differences in Cardiac Repolarization in Mouse Ventricle Circ. Res., August 31, 2001; 89(5): 437 - 444. [Abstract] [Full Text] [PDF]
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Z. Kassiri, C. Zobel, T.-T. T. Nguyen, J. D. Molkentin, and P. H. Backx Reduction of Ito Causes Hypertrophy in Neonatal Rat Ventricular Myocytes Circ. Res., March 22, 2002; 90(5): 578 - 585. [Abstract] [Full Text] [PDF]
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W. Guo, H. Li, F. Aimond, D. C. Johns, K. J. Rhodes, J. S. Trimmer, and J. M. Nerbonne Role of Heteromultimers in the Generation of Myocardial Transient Outward K+ Currents Circ. Res., March 22, 2002; 90(5): 586 - 593. [Abstract] [Full Text] [PDF]
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