Regulation of Ca2+ current in frog ventricular myocytes by the holding potential, c-AMP and frequency

Schouten, V. J. A.; Morad, Martin

doi:10.1007/bf00373135

Cited by 74 publications

(47 citation statements)

References 33 publications

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“…As described by others (Argibay et al, 1988;Tseng, 1988; but see also Schouten & Morad, 1989) and shown in Figure 4, ICa recovery kinetics depended on the membrane holding potential. They were more rapid as the HP was more negative (half a -60 Voltage ( Prepulse potential (mV) (Figure 4a).…”

Section: Effects Of Heptaminol On Ica Recovery From Inactivationsupporting

confidence: 79%

Alteration of the L‐type calcium current in guinea‐pig single ventricular myocytes by heptaminol hydrochloride

Peineau

Mongo

Guennec

et al. 1992

British J Pharmacology

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1 The effects of heptaminol on calcium current amplitude and characteristics were studied in single ventricular myocytes of guinea-pig by use of the whole cell configuration of the patch clamp technique. 2 A concentration-dependent decrease in 'Ca amplitude was observed. At heptaminol concentration as low as 10-6 M, this effect was observed in only two cells (n = 6). At 10-5 M the reduction of ICa was of 30± 15% (n =11). 3 The current recovery from inactivation at -40 mV holding potential (HP) seemed less sensitive to perfusion with heptaminol (> 10-6 M). However, at -80 mV HP the overshoot of the recovery curve was decreased by heptaminol. 4 Both at -40 mV and -80 mV HP, heptaminol (10-' M) significantly increased the steady state inactivation of ICa 5 As previously proposed by others to explain the effects of membrane active substances, the effects of heptaminol may result from alterations in cell membrane properties and possibly from an increase in intracellular free calcium ion concentration.

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Section: Effects Of Heptaminol On Ica Recovery From Inactivationsupporting

confidence: 79%

Alteration of the L‐type calcium current in guinea‐pig single ventricular myocytes by heptaminol hydrochloride

Peineau

Mongo

Guennec

et al. 1992

British J Pharmacology

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“…[22][23][24][25] The results of this study imply that calcium overload may also be partly responsible for AF-induced atrial mechanical dysfunction. Rapid [17][18][19] and irregular 20 depolarization of atrial myocytes as a result of AF results in elevation of cytosolic calcium. This increase in cellular calcium concentration may then serve as the common mediator of AF-induced electrical remodeling (by shortening the atrial refractory period) and AF-induced contractile dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Frequent [17][18][19] and irregular 20 depolarization of atrial myocytes during AF results in elevation of cytosolic calcium. 9 The absence of AF-induced contractile dysfunction in patients pretreated with verapamil suggests that AF-induced cytosolic calcium overload may mediate this acute dysfunction.…”

Section: Possible Mechanismsmentioning

confidence: 99%

Short-Term Effect of Atrial Fibrillation on Atrial Contractile Function in Humans

et al. 1999

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Background-Conversion of chronic atrial fibrillation (AF) is associated with atrial stunning, but the short-term effect of a brief episode of AF on left atrial appendage (LAA) emptying velocity is unknown. The purpose of this study was to determine whether a short episode of AF affects left atrial function and whether verapamil modifies this effect. Methods and Results-The subjects of this study were 19 patients without structural heart disease undergoing an electrophysiology procedure. In 13 patients, LAA emptying velocity was measured by transesophageal echocardiography in the setting of pharmacological autonomic blockade before, during, and after a short episode of AF. During sinus rhythm, the baseline LAA emptying velocity was measured 5 times and averaged. AF was then induced by rapid right atrial pacing. After either spontaneous or electrical conversion, LAA emptying velocity was measured immediately on resumption of sinus rhythm and every minute thereafter. The mean duration of AF was 15.3Ϯ3.8 minutes. The mean baseline emptying velocity was 70Ϯ20 cm/s. The first post-AF emptying velocity was 63Ϯ20 cm/s (Pϭ0.02 versus baseline emptying velocity). The post-AF emptying velocity returned to the baseline emptying velocity value after 3.0 minutes. The mean percent reduction in post-AF emptying velocity was 9.7Ϯ21% (range, 15% increase to 56% decrease). A second group of 6 patients were pretreated with verapamil (0.1-mg/kg IV bolus followed by an infusion of 0.005 mg ⅐ kg Ϫ1 ⅐ min

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“…For example in cardiac ventricular myocytes, the potentiation of L-type current was current dependent (i.e. it depended on the amount of Ca2+ influx) and it could be blocked by intracellular EGTA; it has been attributed to [Ca2+]i-dependent phosphorylation of L-type Ca2+ channels (Argibay, Fischmeister & Hartzell, 1988;Tseng, 1988;Zygmunt & Maylie, 1990; but see Lee, 1987Lee, , 1989Schouten & Morad, 1989 The following results obtained in this study indicated that potentiation crucially depends on voltage-dependent T-type channel inactivation: (1) the extent of potentiation and the steady-state inactivation curve followed a very similar voltage dependence (Fig. 8). (2) Diminution of inactivation by reducing the duration of the pre-pulses reduced in parallel the extent of potentiation.…”

Section: Properties Of the T-type Current Compared To Those In Other mentioning

confidence: 99%

Stimulation‐induced potentiation of T‐type Ca2+ channel currents in myocytes from guinea‐pig coronary artery.

VYa

Isenberg

1991

The Journal of Physiology

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SUMMARY1. Whole-cell Ca2+ channel currents were studied in myocytes isolated from guinea-pig circumflex coronary artery at 36°C and with 10 mM-Ba21 (or Ca2+) as charge carrier. With 180 ms clamp steps from the holding potential of -100 mV, currents at -30 mV were carried mostly through the T-type calcium channels while at positive potentials currents were mostly of the L-type.2. The increase in frequency of pulsing from 0'1 to 2X5 Hz resulted in a reduction of peak inward current ('negative staircase') with the 180 ms pulses to + 10 mV, but in a 2-fold potentiation ('positive staircase') with pulses to -30 mV. T-type currents and their frequency-mediated potentiation did not change significantly when Ba2+ was substituted by Ca2+ or Sr2+.3. Potentiation of T-type currents was further analysed with a paired-pulse protocol: at a basal frequency of 01 Hz, a pre-pulse (inducing current I,) was followed by a 200 ms repolarization to -100 mV and a test pulse (inducing current I2). The potentiation could only be recorded using test pulses depolarizing the membrane to potentials between -40 and -10 mV; at more positive test potentials it was masked by the depressant effect of pre-pulses on the L-type current.4. Potentiation of I2 by 200 ms pre-pulses started at pre-pulse potentials more positive than -60 mV and saturated at -20 mV (I2 potentiated by a factor 2-4). Between -20 and + 130 mV the potentiation was not dependent on the pre-pulse potential suggesting that the influx of Ba2+ or Ca2+ is not required for this effect. Potentiation of I2 by a 10 s pre-pulse followed the voltage dependence of the steadystate inactivation curve of the T-type Ca2+ channel; potentiation became visible at potentials more positive than -80 mV and saturated at about -50 mV.5. When changing the interval between two identical 200 ms pulses, the T-type current was found to recover completely from inactivation within 40 ms at -100 mV; at intervals of 160-320 ms maximal potentiation of I2 occurred.6. With pre-pulses shorter than 200 ms, potentiation became attenuated when inactivation became less complete. When the potential during the interval between the pulses was -80 instead of -100 mV, maximal potentiation was reduced (I2 potentiated by a factor of 1-3 instead of 2-2) and occurred later (1-28 s).7. Potentiated T-type currents inactivated faster. In the double-pulse experiments when peak ratio (12/I1) was 1-98+0417, the current during the second pulse showed MS 9156 V. YA. GANITKEVICH AND G. ISENBERG a single exponential time course of inactivation with a time constant of 5-6 + 0 7 ms, while the current during the first pulse had a time constant of inactivation of 14-5 + 1P5 ms. Due to faster inactivation the second current (I2) transported nearly the same charge compared to first current (I,) (charge ratio 0-94+0416). Unlike the current amplitude, the transported charge did not exhibit a transient potentiation when the pulse interval was increased. 8. At -100 mV, T-type Ca2+ channels recovered faster from steady-state inactivation than L-t...

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Regulation of Ca2+ current in frog ventricular myocytes by the holding potential, c-AMP and frequency

Cited by 74 publications

References 33 publications

Alteration of the L‐type calcium current in guinea‐pig single ventricular myocytes by heptaminol hydrochloride

Alteration of the L‐type calcium current in guinea‐pig single ventricular myocytes by heptaminol hydrochloride

Short-Term Effect of Atrial Fibrillation on Atrial Contractile Function in Humans

Stimulation‐induced potentiation of T‐type Ca2+ channel currents in myocytes from guinea‐pig coronary artery.

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