Comparison of sodium‐calcium exchanger and transient inward currents in single cells from rabbit ventricle.

W, Giles; Shimoni, Y.

doi:10.1113/jphysiol.1989.sp017813

Cited by 48 publications

(17 citation statements)

References 50 publications

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“…This is similar to findings in ventricular cells of guinea pig 25,29 but contrasts with observations made in ventricular cells of dog, 11 rabbit, 12 sheep, 14 and ferret. 30 In these species, I ti consisted of both I Cl(Ca) and I Na/Ca .…”

Section: Species-dependency Of Ionic Nature Of Dadscontrasting

confidence: 53%

Ionic Mechanism of Delayed Afterdepolarizations in Ventricular Cells Isolated From Human End-Stage Failing Hearts

et al. 2001

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Background-Animal studies have shown that the Ca 2ϩ -activated Cl Ϫ current (I Cl(Ca) ) and the Na ϩ /Ca 2ϩ exchange current (I Na/Ca ) contribute to the transient inward current (I ti ). I ti is responsible for the proarrhythmic delayed afterdepolarizations (DADs). We investigated the ionic mechanism of I ti and DADs in human cardiac cells. Methods and Results-Human ventricular cells were enzymatically isolated from explanted hearts of patients with end-stage heart failure and studied with patch-clamp methodology. I ti s were elicited in the presence of 1 mol/L norepinephrine by trains of repetitive depolarizations from Ϫ80 to ϩ50 mV. DADs were induced in the presence of 1 mol/L norepinephrine at a stimulus frequency of 1 Hz. I ti currents were inwardly directed over the voltage range between Ϫ110 and ϩ 50 mV. Neither the Cl Ϫ channel blocker 4,4Ј-diisothiocyanatostilbene-2,2Ј-disulfonic acid nor changes in [Cl Ϫ ] i affected I ti or DAD amplitude. This excludes an important role for I Cl(Ca) . Blockade of Na ϩ /Ca

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Section: Species-dependency Of Ionic Nature Of Dadscontrasting

confidence: 53%

Ionic Mechanism of Delayed Afterdepolarizations in Ventricular Cells Isolated From Human End-Stage Failing Hearts

et al. 2001

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“…In rabbits, however, the arrhythmogenic role of this mechanism has not been clearly demonstrated. In addition, the distinct nature of ITI and the Na'-Ca2' exchange mechanism in rabbit ventricular cells has been suggested by Giles & Shimoni (1989). In contrast, in the same preparation, Laflamme & Becker (1996) demonstrated inward currents during spontaneous [Ca2+]i oscillations when Cl-was absent from both the external and the internal solutions.…”

Section: Cell Isolationmentioning

confidence: 92%

Calcium‐activated transient membrane currents are carried mainly by chloride ions in isolated atrial, ventricular and Purkinje cells of rabbit heart

Szigeti

Rusznák

Kovács

et al. 1998

Experimental Physiology

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SUMMARYUnder physiological conditions, calcium-dependent ([Ca2+] -dependent) Cl-currents (ICI(Ca)) have been suggested to participate in the repolarizing processes. In this paper, the possible contribution of ICl(Ca) to transient inward currents and, hence to arrhythmias, has been studied in myocytes from the working myocardium and from the conductive system. Single atrial, ventricular and Purkinje cells, isolated enzymatically from rabbit heart, have been studied under whole-cell voltage-clamp and were internally perfused with the fluorescent Ca2+ indicator, fura-2 (100 /sM). Ca + release from the sarcoplasmic reticulum was either induced by external application of caffeine or occurred spontaneously in Ca2+-overloaded cells. Membrane currents accompanying Ca2+ transients showed linear current-voltage characteristics between -60 and +80 mV as evidenced from fast voltage ramps. When intra-and extracellular Cl-concentrations were kept symmetrical in the absence of the Na+-Ca2' exchange mechanism, transient currents had a reversal potential close to 0 mV.

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“…The delayed inwardly directed tail currents similar to the current investigated in this work have so far been identified in isolated cells of various species including rat (Mitchell et al 1984), guinea-pig (Fedida et al 1987;Beuckelmann & Wier, 1988), frog (Hume, 1987;Campbell et al 1988) and rabbit (Giles & Shimoni, 1989b). The relation between delayed tail current and contraction was studied by Fedida et al (1987) in guinea-pig ventricular myocytes.…”

Section: Relation To Calcium Currentsmentioning

confidence: 99%

A contraction‐related component of slow inward current in dog ventricular muscle and its relation to Na(+)‐Ca2+ exchange.

Šimurda

Šimurdová

Bravený

et al. 1992

The Journal of Physiology

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SUMMARY1. The slow inward current component related to contraction (Ii,) was studied in voltage clamp experiments on canine ventricular trabeculae at 30 0C with the aims of (a) estimating its relation to electrogenic Na+-Ca2+ exchange and (b) comparing it with similar currents as reported in cardiac myocytes.2. Ii, may be recorded under conditions of augmented contractility in response to depolarizing pulses below the threshold of the classic slow inward current (presumably mediated by L-type Ca2+ channels). In responses to identical depolarizing clamp pulses the peak value of 1sic is directly related to the amplitude of contraction (Fmax). Isic peaks about 60 ms after the onset of depolarization and declines with a half-time of about 110 ms.3. The voltage threshold of Isic activation is the same as the threshold of contraction. The positive inotropic clamp preconditions shift both thresholds to more negative values of membrane voltage, i.e. below the threshold of the classic slow inward current.4. Ij, may also be recorded as a slowly decaying inwardly directed current 'tail' after depolarizing pulses. In this representation the peak value of I~j, changes with duration of the depolarizing pulses, again in parallel with Fmax. In response to pulses shorter than 100 ms both variables increase with depolarization time. If initial conditions remain constant, further prolongation of the pulse does not significantly influence either one (tail currents follow a common envelope).5. Ij, differs from classic slow inward current by: (a) its direct relation to contraction, (b) the slower decay of the current tail on repolarization, (c) slower restitution corresponding to the mechanical restitution, (d) its relative insensitivity to Ca2+-blocking agents (the decrease of I.ij is secondary to the negative inotropic effect) and (e) its disappearance after Sr2+ substitution for Ca2+.6. The manifestations ofIsic in multicellular preparations do not differ significantly from those reported in isolated myocytes (in contrast to calcium current).7.

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Comparison of sodium‐calcium exchanger and transient inward currents in single cells from rabbit ventricle.

Cited by 48 publications

References 50 publications

Ionic Mechanism of Delayed Afterdepolarizations in Ventricular Cells Isolated From Human End-Stage Failing Hearts

Ionic Mechanism of Delayed Afterdepolarizations in Ventricular Cells Isolated From Human End-Stage Failing Hearts

Calcium‐activated transient membrane currents are carried mainly by chloride ions in isolated atrial, ventricular and Purkinje cells of rabbit heart

A contraction‐related component of slow inward current in dog ventricular muscle and its relation to Na(+)‐Ca2+ exchange.

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