Sodium current kinetics in intact rat papillary muscle: measurements with the loose‐patch‐clamp technique.

Antoni, H.; Böcker, D; Eickhorn, Roland

doi:10.1113/jphysiol.1988.sp017376

Cited by 38 publications

(15 citation statements)

References 27 publications

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“…This 89.8% reduction of the CssIV-sensitive sodium current by 181 nM TTX indicates an EC 50 for TTX of 20.6 nM, assuming one-to-one binding. This EC 50 value is markedly lower than that typically reported in cardiac preparations (23)(24)(25) and similar to that reported for Na v 1.1 (9.6 nM TTX, 26), Na v 1.3 (1.8 nM TTX, 22), and Na v 1.6 (2.5 nM TTX, 17) when expressed in Xenopus oocytes or cell lines. Therefore, this CssIV-sensitive current is likely to be conducted by Na v 1.1, Na v 1.3, and Na v 1.6.…”

Section: (D -H)supporting

confidence: 85%

“…To test this hypothesis, we administered 100 or 200 nM TTX to isolated working mouse and guinea pig hearts. These TTX concentrations are expected to block 83 and 91% of neuronal sodium channels, respectively (assuming an EC 50 of 20.6 nM) and have little effect on the cardiac Na v 1.5 isoform (1.5 and 3% block for 100 and 200 nM, respectively, assuming an EC 50 of 6.3 M in 122 mM sodium concentration (25). Thus, these TTX concentrations should isolate physiological effects of neuronal Na v 1.1, Na v 1.3, and Na v 1.6 from those of cardiac Na v 1.5 sodium channels.…”

Section: Role Of Brain-type Sodium Channels In Cardiac Contractility mentioning

confidence: 99%

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An unexpected role for brain-type sodium channels in coupling of cell surface depolarization to contraction in the heart

Maier

Westenbroek

Schenkman

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

270

250

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Voltage-gated sodium channels composed of pore-forming ␣ and auxiliary ␤ subunits are responsible for the rising phase of the action potential in cardiac muscle, but the functional roles of distinct sodium channel subtypes have not been clearly defined. Immunocytochemical studies show that the principal cardiac poreforming ␣ subunit isoform Nav1.5 is preferentially localized in intercalated disks, whereas the brain ␣ subunit isoforms Nav1.1, Nav1.3, and Nav1.6 are localized in the transverse tubules. Sodium currents due to the highly tetrodotoxin (TTX)-sensitive brain isoforms in the transverse tubules are small and are detectable only after activation with ␤ scorpion toxin. Nevertheless, they play an important role in coupling depolarization of the cell surface membrane to contraction, because low TTX concentrations reduce left ventricular function. Our results suggest that the principal cardiac isoform in the intercalated disks is primarily responsible for action potential conduction between cells and reveal an unexpected role for brain sodium channel isoforms in the transverse tubules in coupling electrical excitation to contraction in cardiac muscle.

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Section: (D -H)supporting

confidence: 85%

Section: Role Of Brain-type Sodium Channels In Cardiac Contractility mentioning

confidence: 99%

An unexpected role for brain-type sodium channels in coupling of cell surface depolarization to contraction in the heart

Maier

Westenbroek

Schenkman

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

270

250

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“…From analyses of the steady-state inactivation and inactivation kinetics of INa in this preparation, we have concluded as follows: (1) (Brown, Lee & Powell, 1981;Cachelin, Depeyer, Kokubun & Reuter, 1983;Follmer, Ten Eick & Yeh, 1987;Antoni et al 1988) and in nerve cells (Chiu, 1977;Meves, 1978 Calcium currents (ICa) The properties of the Ca2" channels in this preparation were similar to those in sympathetic neurones of the chick (Marchetti, Carbone & Lux, 1986), rat (Wanke, Ferroni Malgaroli, Ambrosini, Pozzan & Meldolesi, 1987) and frog (Jones & Marks, 1989). They have the same threshold for activation (the range of -40 to -30 mV) and maximum values in I-V relationships (the range of 0 to + 10 mV) at 2-5 mm…”

Section: Discussionmentioning

confidence: 99%

Voltage‐dependent ionic currents in dissociated paratracheal ganglion cells of the rat.

Aibara

Ebihara

Akaike

1992

The Journal of Physiology

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SUMMARY1. Conventional whole-cell voltage-clamp technique was used to study the electrophysiological and pharmacological properties of voltage-dependent Na', K+ and Ca21 channels in parasympathetic neurones enzymatically dissociated from the paratracheal ganglia of rat trachea. The voltage-dependent Na+, K+ and Ca2+ currents (INa' IK and ICa) were separated by the use of ion subtraction and pharmacological treatments.2. INa was activated by a step depolarization more positive than -50 mV and fully activated at positive potentials more than + 10 mV. The inactivation phase of INa consisted offast and slow exponential components (Tif and Tis' respectively). The rif and r.i were voltage dependent and decreased with a more positive step pulse.3. The time course for recovery of INa from the complete inactivation exhibited two exponential processes.4. The reversal potential of INa was equal to the Na+ equilibrium potential (ENa) and resembled a simple Na+ electrode depending only on external Na+ concentration.5. Tetrodotoxin (TTX) reduced INa without affecting the current kinetics in a concentration-dependent manner, and the concentration of half-maximal inhibition (IC50) was 6 x 10' M. There was no TTX-resistant component of INa in any of the cells tested.6. Scorpion toxin increased the peak amplitude of INa and prolonged the inactivation phase in a time-and concentration-dependent manner. In the presence of toxin, both ris and the fractional contribution of the slow current component to total INa increased concentration dependently.7. High-threshold (L-type) ICa was activated by a step depolarization more positive than -30 mV and reached a peak at near 0 mV in the external solution with 2-5 mm Ca2+. The current was inactivated to only a small extent (< 10%) during 100 ms of depolarizing step pulse. There was no low-threshold (T-type) ICa in this preparation.8 K. AIBARA, S. EBIHARA AND KY AKAIKE 9. The inactivation process of the L-type ICa was dependent on Ca2+ influxes (ICadependent inactivation).10. Relative maximum peak currents of divalent cations passing through the Ltype Ca2+ channels were in the order of IBa > ICa > ISr.11. Organic and inorganic Ca2+ antagonists blocked the ICa in a concentrationdependent manner. The order of inhibition was wo-conotoxin > flunarizine > nimodipine > D600 > diltiazem > amiloride for organic blockers and La3+ > Cd2+ > Ni2+ > Co2+ for inorganic ones.12. Three types of IK were observed; i.e. an inwardly rectifying current, a delayed outward current ('KD) and a transient outward current ('A) 13. Depolarizing pulses from a holding potential (VH) of -90 mV elicited K+ currents which seemed to suggest the existence of two distinct cell types. The 'A was observed in the majority of cells (44 out of 63 cells). The IKD was elicited in all cells tested.14. 'KD was activated by step pulses more positive than -20 mV, slowly inactivated (T > 1 s) and reduced by adding tetraethylammonium (IC50 was 4 4 mM).15. The IA was characterized by a rapid activation and inactivation. The amplitude o...

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“…Low concentration of TTX, 100-200 nM, inhibited Na v 1.1, while full inhibition of Na v 1.5 required more than 20-30 µM TTX (Antoni et al 1988;Maier et al 2003;Lei et al 2004). These pharmacological treatments could easily separate Na v 1.1 from Na v 1.5.…”

Section: Discussionmentioning

confidence: 99%

Contribution of Nav1.1 to cellular synchronization and automaticity in spontaneous beating cultured neonatal rat ventricular cells

Masumiya¹

2011

gpb

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Abstract. Two factors of cell coupling influence cellular synchronization and automaticity: gap junction coupling and ion channels activity. However, the role of Na + channel isoforms underlying cellto-cell interaction and cellular automaticity is not well understood. To address these questions, we studied mRNA expression of Na + channel isoforms and the effects of TTX on spontaneously beating cultured ventricle cells. Using RT-PCR technique we demonstrated the presence of Na v 1.1 and Na v 1.5 channels. The reduction of Na v 1.1 channel activity disturbed cell-to-cell interaction and changed beating rates. Thus, Na v 1.1 channel is involved in cellular synchronization and automaticity.

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Sodium current kinetics in intact rat papillary muscle: measurements with the loose‐patch‐clamp technique.

Cited by 38 publications

References 27 publications

An unexpected role for brain-type sodium channels in coupling of cell surface depolarization to contraction in the heart

An unexpected role for brain-type sodium channels in coupling of cell surface depolarization to contraction in the heart

Voltage‐dependent ionic currents in dissociated paratracheal ganglion cells of the rat.

Contribution of Nav1.1 to cellular synchronization and automaticity in spontaneous beating cultured neonatal rat ventricular cells

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