Interconversion between distinct gating pathways of the high threshold calcium channel in rat ventricular myocytes.

Richard, Sylvain; Charnet, Pierre; Nerbonne, Jeanne M.

doi:10.1113/jphysiol.1993.sp019551

Cited by 39 publications

(49 citation statements)

References 45 publications

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“…In cardiac cells, it has been reported that a channel opening similar to mode 2 gating is induced by high concentrations of 13-adrenergic agonists (Yue et al, 1990) and is probably due to the complete phosphorylation of the Ca 2+ channel protein (Ono and Fozzard, 1993). Furthermore, it has recently been shown that potentiation (increase in size of the peak amplitude and slower inactivation) of Ca 2 § current induced by repetitive depolarization (e.g., Noble and Shimoni, 1981;Mitra and Morad, 1986;Richard, Charnet, and Nerbonne, 1993) is linked to phosphorylation processes, perhaps Ca 2+ and cyclic AMP-dependent phosphorylation (Tiaho, Piot, Nargeot, and Richard, 1994). These facts have opened a possibility that mode 2-like gating mechanisms may occur even under physiological conditions.…”

Section: Discussionmentioning

confidence: 99%

Interaction of Ca2+ agonist and depolarization on Ca2+ channel current in guinea pig detrusor cells [published erratum appears in J Gen Physiiol 1996 Jun;107(6):755]

Nakayama

Brading

1995

The Journal of General Physiology

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The interaction of large depolarization and dihydropyridine Ca 2+ agonists, both of which are known to enhance L-type Ca 2+ channel current, was examined using a conventional whole-cell clamp technique. In guinea pig detrusor cells, only L-type Ca 2+ channels occur. A second open state (long open state: 02) of the Ca ~+ channels develops during large depolarization (at +80 mV, without Ca 2+ agonists). This was judged from lack of inactivation of the Ca 2+ channel current during the large depolarizing steps (5 s) and slowly deactivating inward tail currents (= 10--15 ms) upon repolarization of the cell membrane to the holding potential (-60 mV). Application of Bay K 8644 (in 2.4 mM Ca2+-containing solutions) increased the amplitude of the Ca 2+ currents evoked by simple depolarizations, and made it possible to observe inward tail currents (= 2.5-5 ms at -60 mV). The open state induced by large depolarization (O2") in the Bay K 8644 also seemed hardly to inactivate. After preconditioning with large depolarizing steps, the decay time course of the inward tail currents upon repolarization to the holding potential (-60 mV) was significantly slowed, and could be fitted reasonably with two exponentials. The fast and slow time constants were 10 and 45 ms, respectively, after 2 s preconditioning depolarizations. Qualitatively the same results were obtained using Ba 2+ as a charge carrier. Although the amplitudes of the inward currents observed in the test step and the subsequent repolarization to the holding potential were decreased in the same manner by additional application of nifedipine (in the presence of Bay K 8644), the very slow deactivation time course of the tail current was little changed. The additive enhancement by large depolarization and Ca ~ § agonists of the inward tail current implies that two mechanisms separately induce long opening of the Ca 2+ channels: i.e., that there are four open states.

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Section: Discussionmentioning

confidence: 99%

Interaction of Ca2+ agonist and depolarization on Ca2+ channel current in guinea pig detrusor cells [published erratum appears in J Gen Physiiol 1996 Jun;107(6):755]

Nakayama

Brading

1995

The Journal of General Physiology

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“…This was described first in frog atrium (Noble and Shimoni, 1981), and then in rat (Richard et al, 1990;Richard et al, 1993), guinea-pig (Mitra and Morad, 1986;Lee, 1987;Fedida et al, 1988a;Fedida et al, 1988b;Zygmunt and Maylie, 1990), rabbit (Hryshko and Bers, 1990), ferret dog (Tseng, 1988) and human (Piot et al, 1996) cardiomyocytes, although a pronounced decrease of I Ca has been observed in mouse (Sipido et al, 1998b) in which the decrease might reflect insufficient time to recover from voltage dependent inactivation.…”

Section: Facilitationmentioning

confidence: 98%

Ca2+ currents in cardiac myocytes: Old story, new insights

Brette

Leroy

Guennec

et al. 2006

Progress in Biophysics and Molecular Biology

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“…Repetitive depolarization, for example, produces channel inactivation when cells are stimulated from depolarized membrane holding potentials (Mitchell, Powell, Terrar & Twist, 1985;Fedida, Noble & Spindler, 1988a, b;Peineau, Garnier & Argibay, 1992;Richard, Charnet & Nerbonne, 1993). Ca2"-dependent inactivation (Mitchell et al 1985) or incomplete voltagedependent reactivation (Hryshko & Bers, 1990;Peineau et al 1992;Richard et al 1993) of Ca2" channels have been suggested to account for the decrease of ICa, Alternatively, repetitive depolarization can produce potentiation of Ca2+ channel activity (Noble & Schimoni, 1981;Mitra & Morad, 1986;Lee, 1987;Fedida et al 1988a, b;Tseng, 1988;Schouten & Morad, 1989; Richard, Tiaho, Charnet, Nargeot & Nerbonne, 1990;Zygmunt & Maylie, 1990;Peineau et al 1992) when ICa is evoked from negative holding potentials (<-50 mV). The molecular mechanisms underlying this potentiation, known as facilitation, are also a matter of debate.…”

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confidence: 99%

Regulation of the frequency‐dependent facilitation of L‐type Ca2+ currents in rat ventricular myocytes.

Tiaho

Piot

Nargeot

et al. 1994

The Journal of Physiology

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1. An increase in the rate of stimulation induces an augmentation of L-type Ca2+ currents (Ica) and concomitant slowing of current decay in rat ventricular cells. This facilitation is quasi immediate (1-3 s), graded with the rate of stimulation, and occurs only from negative holding potentials. We investigated this effect using trains of stimulation at 1 Hz and the whole-cell patch-clamp technique (18-22°C).2. The decay of Ica is normally bi-exponential and comprises fast and slow current components (Ica fe and Ica,sc respectively). Facilitation of Ica was observed only when ica,fc was predominant.3. Facilitation developed during the run-up of 'Ca with the interconversion of Ica,sc into ica,fC and vanished during the run-down of 'Ca with the loss of 'ca,fc. Ni2" (300 /AM) and nifedipine (1 M) suppressed facilitation owing to the preferential inhibition of Ica,fc-4. Facilitation of Ica was not altered (when present) or favoured (when absent) by the cAMP-dependent phosphorylation of Ca2" channels promoted by isoprenaline or by intracellular application of cAMP or of the catalytic subunit of protein kinase A (C-sub). A similar effect was observed when the dihydropyridine agonist Bay K 8644 was applied.In both cases, facilitation was linked to a preferential increase of 'ca,fe 5. Following intracellular application of inhibitors of protein kinase A in combination with a non-hydrolysable ATP analogue, Ica consisted predominantly of Ica,sc and no facilitation was observed. The calmodulin antagonist naphthalenesulphonamide had no effect on facilitation. 6. When Bay K 8644 was applied in combination with isoprenaline, cAMP or C-sub, the decay of Ica was slowed with the predominant development of Ica,s'c and facilitation of Ica was nearly abolished. Facilitation also depended on extracellular Ca2+, and was suppressed when Ba2" replaced Ca2+ as the permeating ion.7. When no EGTA was included in the patch pipette, facilitation was not further enhanced but a use-dependent decrease of Ica frequently occurred. When BAPTA was used in place of EGTA, the rate of inactivation of Ica was reduced and facilitation was abolished.8. In conclusion, the facilitation of Ica that reflects a voltage-driven interconversion of Ica,fe into Icasc is also regulated by Ca2' and by cAMP-dependent phosphorylation. The presence of the gating pattern typified by 'Ca fe is required. Ca21 may exert its effect near the inner pore of the Ca21 channel protein and control the distribution between the closed states of the two gating pathways.

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Interconversion between distinct gating pathways of the high threshold calcium channel in rat ventricular myocytes.

Abstract: 9. Experimental testing of the predictions of the parallel pathway gating model suggests that the experimentally observed time-and voltage-dependent interconversions between the two gating pathways only occur via the closed states of the channel.

Cited by 39 publications

References 45 publications

Interaction of Ca2+ agonist and depolarization on Ca2+ channel current in guinea pig detrusor cells [published erratum appears in J Gen Physiiol 1996 Jun;107(6):755]

Interaction of Ca2+ agonist and depolarization on Ca2+ channel current in guinea pig detrusor cells [published erratum appears in J Gen Physiiol 1996 Jun;107(6):755]

Ca2+ currents in cardiac myocytes: Old story, new insights

Regulation of the frequency‐dependent facilitation of L‐type Ca2+ currents in rat ventricular myocytes.

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