Ion transfer characteristics of the calcium current in bull‐frog atrial myocytes.

Campbell, Donald L.; Giles, Wayne R.; Shibata, Erwin F.

doi:10.1113/jphysiol.1988.sp017248

Cited by 39 publications

(49 citation statements)

References 85 publications

(174 reference statements)

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“…The experimental methods, compositions of solutions, electronic apparatus and techniques for data analysis were all the same as those described in the first paper of this series (Campbell, Giles & Shibata, 1988b).…”

Section: Methodsmentioning

confidence: 99%

“…The 10 ms gap between the P1 pre-pulse and P2 test pulse was applied in an attempt to reset the activation variable ('dx') back to its initial value at the beginning of the P, pulse, so as not to underestimate any decrease in P2 current size due to inactivation produced by P, (cf. Gillespie & Meves, 1980 (Nathan, Clark, Kanai & Giles, 1988;Campbell et al 1988b (Fig. 4).…”

Section: Methodsmentioning

confidence: 99%

“…As described by Campbell et al (1988b) and Clark & Giles (1987) the 'Discrete' curve-fitting program (Provencher, 1976) was used in the kinetic analysis of ICa for determination of (i) the number of exponential components and (ii) the values of time constant(s) associated with each component. The program requires only raw data as its input: it does not use any initial guesses of either the number of exponential component(s) or their initial value(s).…”

Section: Methodsmentioning

confidence: 99%

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Inactivation of calcium current in bull‐frog atrial myocytes.

Campbell

Giles

Hume

et al. 1988

The Journal of Physiology

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SUMMARY1. A single-microelectrode technique has been used to study the voltage dependence and the kinetics of inactivation and reactivation of a tetrodotoxinresistant inward current (ICa) in single cells from bull-frog atrium.2. In most cases the kinetics of both inactivation and reactivation can be well described as a single-exponential process.3. Several different observations indicate that inactivation of ICa in these cells is controlled by both voltage-dependent and current-dependent processes, as has been demonstrated previously in heart (Kass & Sanguinetti, 1984;Lee, Marban & Tsien, 1985) and in other tissues (Hagiwara & Byerly, 1981;Tsien, 1983;Eckert & Chad, 1984

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Inactivation of calcium current in bull‐frog atrial myocytes.

Campbell

Giles

Hume

et al. 1988

The Journal of Physiology

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“…These results have been explained previously by postulating the presence of a saturable binding site within, but close to the outer surface of, the Ca2+ channel to which cations must bind before entering the Ca2+ channel. Barium is thought to bind less strongly and, therefore, permeates through the channel with a greater conductance Ganitkevich et al 1988;Campbell et al 1988a (Lee & Tsien, 1983) . Ureteral cells were always perfused with 3 mM-EGTA so that the internal Ca2+ concentration would be extremely low.…”

Section: Co2± Insensitive Inward Currentmentioning

confidence: 99%

The whole‐cell Ca2+ channel current in single smooth muscle cells of the guinea‐pig ureter.

Lang

1990

The Journal of Physiology

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SUMMARY1. Calcium channel currents were recorded in single, enzymatically isolated smooth muscle cells of the guinea-pig ureter using a single-electrode whole-cell voltage clamp technique. Calcium and barium currents through voltage-activated Ca2+ channels were recorded in cells dialysed with Cs+-or Na+-containing saline which suppressed K+ currents.2. Inward currents in Ca2+ (1P5-75 mM) or Ba2+ (1P5-75 mM) were recorded at potentials positive to -50 to -30 mV. Inward currents were maximal at 0 mV in 1-5 mM-Ca2+ and at + 10 mV in 7-5 mM-Ba2t. Current flow through Ca2+ channels in Cs+-filled cells (in 1-5 mM-Ca2+ or 7-5 mM-Ba2+) changed from inward to outward at potentials positive to + 70 mV. In Na+-filled cells this reversal potential was between + 50 and + 60 mV.3. Replacing Ca2+ or Ba2+ with Co2+ (1P5 mM) blocked all inward current flow through these Ca2+ channels; outward currents at potentials positive to +40 mV, however, were increased. Cadmium (100 uM) and nifedipine (0-1-10 ftM) reduced both inward and outward current flow.4. Calcium channel activation showed a sigmoidal relationship with membrane potential; the potential of half-maximal activation was -8-4 mV in 1-5 mM-Ca2+ and -10-8 mV in 7-5 mM-Ba2+. The maximum membrane conductance to Ca2+ (in 1-5 mM-Ca2+) was 2-57 nS/cell or approximately 0 05 mS/cm2.5. Evidence for a voltage-dependent inactivation mechanism included (a) the time-dependent relaxation of the outward currents at potentials positive to the reversal potential and (b) a steady-state inactivation (foo(v)) vs. membrane potential relationship (in 7.5 mM-Ba2+) which ranged between -80 and 0 mV, with a halfmaximal availability at -40 5 mV.6. The voltage dependencies of the inward current elicited from -80 and -30 mV were similar, suggesting that depolarization activated only L-type Ca2+ channels.7. It was concluded that the processes controlling the time course of the Ca2+ current in single ureteral cells bathed in physiological concentrations of Ca2+ were mostly voltage-dependent.

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“…Divalent cations (CaC12 and BaCl2) were added to the Et4N' solution without osmotic compensation. Tetrodotoxin (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) AM) was also present in selected experiments. In phosphorylation inhibition experiments (see Fig.…”

mentioning

confidence: 95%

Modulation of L-type calcium channels by sodium ions.

Balke

Wier

1992

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

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It is universally believed that the removal of external sodium ions is without effect on calcium current. We now report that in enzymatically isolated guinea pig ventricular cells, the replacement of external sodium ions with certain other cations causes a 3-to 6-fold increase in peak L-type calcium current. The increase in current is reversibly blocked by L-type calcium-channel antagonists, not mediated by changes in internal calcium, and is inhibited by intracellular 5'-adenylyl imidodiphosphate, a nonhydrolyzable ATP analogue. The effects of sodium removal (and isoproterenol) were almost completely blocked by intracellular application of a specific (peptide) inhibitor of cAMP-dependent protein kinase. These experiments demonstrate a previously unknown effect of sodium ions to modulate calcium-channel phosphorylation via cAMP-dependent protein kinase.

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Ion transfer characteristics of the calcium current in bull‐frog atrial myocytes.

Cited by 39 publications

References 85 publications

Inactivation of calcium current in bull‐frog atrial myocytes.

Inactivation of calcium current in bull‐frog atrial myocytes.

The whole‐cell Ca2+ channel current in single smooth muscle cells of the guinea‐pig ureter.

Modulation of L-type calcium channels by sodium ions.

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