The action of acetylcholine on background conductance in frog atrial trabeculae.

Garnier, D; Nargeot, Joël; Ojeda, Carlos; Rougier, O

doi:10.1113/jphysiol.1978.sp012154

Cited by 90 publications

(47 citation statements)

References 31 publications

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“…An important question to answer was whether the properties of this conductance are superimposable on those of the pre-existing inward rectifier iK1 (Garnier et al 1978;Ojeda et al 1981 ;Argibay et al 1983), or whether the ACh-sensitive current presents characteristics which suggest that it is different from iK1 (Noma & Trautwein, 1978;Sakmann et al 1983).…”

Section: Discussionmentioning

confidence: 99%

Characterization of the acetylcholine‐induced potassium current in rabbit cardiac Purkinje fibres.

Carmeliet¹,

Mubagwa²

1986

The Journal of Physiology

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SUMMARY1. Acetylcholine (ACh) induces a K+ current in rabbit cardiac Purkinje fibres. The question was studied whether ACh produces this effect by modifying the properties of K+ channels pre-existing in the absence of the neurotransmitter or whether it induces the formation of a different type of K+ channels.2. The relaxation properties of the ACh-induced current and its blockade by Cs+ and Ba2+ have been investigated using voltage clamp.3. During hyperpolarizing or depolarizing voltage pulses of moderate amplitude, the ACh-induced current is time independent. For large voltage pulses, time-dependent changes of the ACh-induced current are observed. These latter changes can be explained by intercellular K+ accumulation/depletion phenomena or by the effects of ACh on time-dependent currents (e.g. the late outward current, ix).4. Cs+ and Ba2+ block the ACh-induced current. The block produced by 20 mM-Cs+ is instantaneous and increases with hyperpolarization, i.e. it is voltage dependent. The block produced by Ba2+ at high concentrations (> 1 mM) is also instantaneous but complete at all potentials studied, and thus voltage independent. At these concentrations, either ion also blocks the background inward rectifier (iKi) current in a similar way.5. Low [Ba2+] (< 0-1 mM) cause a block of the ACh-induced current which is instantaneous and little voltage dependent. The block of iK1 in contrast is time and voltage dependent for the same concentrations. These results indicate that the ACh-induced K+ current is different from the background iK1 current.

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Section: Discussionmentioning

confidence: 99%

Characterization of the acetylcholine‐induced potassium current in rabbit cardiac Purkinje fibres.

Carmeliet¹,

Mubagwa²

1986

The Journal of Physiology

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“…(1) ACh might produce its effects by modulating the properties of a pre-existing channel (Ten Eick et al 1976;Garnier et al 1978;Ojeda et al 1981 ;Argibay et al 1983). (2) Alternatively, ACh might increase K+ conductance by inducing the formation or opening of a new type of channel which does not 214 ACETYLCHOLINE AND PURKINJE FIBRES contribute to the membrane K+ conductance in the absence of agonist (Noma & Trautwein, 1978;Sakmann et al 1983).…”

Section: Discussionmentioning

confidence: 99%

Changes by acetylcholine of membrane currents in rabbit cardiac Purkinje fibres.

Carmeliet¹,

Mubagwa²

1986

The Journal of Physiology

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SUMMARY1. The ionic mechanisms underlying the effects of acetylcholine (ACh) on electrophysiological properties of rabbit cardiac Purkinje fibres have been analysed using the two-micro-electrode voltage-clamp technique on short preparations.2. In normal Tyrode solution, ACh shifted the membrane currents in the outward direction at potentials positive to the K+ equilibrium potential, EK, and in the inward direction at potentials negative to EK. When ACh effects were studied in various [K+].the reversal potential for the ACh-induced current was changed in a way expected for a pure K+ electrode. The results indicate an increase of an inward-rectifying K+ conductance by ACh.3. ACh also decreased the magnitude of the late outward current (ix). The activation curve for this current was not modified, but the fully activated current was decreased. The effect of ACh on ix was more pronounced in the presence of catecholamines.4. The slow inward current (isi) was not changed by ACh in control conditions. However, the increase produced by f-adrenergic stimulation in this current was suppressed by ACh in a concentration-dependent way.

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“…When vagal nerve fibers are stimulated at a low frequency, the discrepancy might be explained by differences between the chronotropic and inotropic fade responses. That is, the fade of the chronotropic response to cholinergic intervention is rarely induced by postjunctional mechanisms at the pacemaker cells (OSTERRIEDER et al, 1982;CARPENTIER et al, 1984; but the fade of the inotropic response is mainly induced at the atrial muscle cells (GARNIER et al, 1978;GLITSCH and POTT, 1978;GERTJEGERDES et al, 1979;TOKIMASA et al, 1980;MARTIN et al, 1982). In the present study, an additional fade of the inotropic response induced by an inhibition of AChE was not demonstrated.…”

Section: Discussionmentioning

confidence: 48%

“…The fade of the inotropic response to parasympathetic nerve stimulation might be induced by one or a combination of the following mechanisms: (a) a reduction of ACh release ; (b) muscarinic receptor desensitization (JALIFE et al, 1980;TOKIMASA et al, 1980); (c) a post-receptor mechanism, e.g., changes in intracellular calcium movement (GERTJEGERDES et al, 1979;MARTIN et al, 1982);and/or (d) an augmentation of the washout of ACh from neuroeffector gaps. In the present study, we focused on the role of ACh at the neuroeffector junction in the fade response.…”

Section: Discussionmentioning

confidence: 99%

Fade responses at neuroeffector junction to vagal stimulation in the isolated, blood-perfused dog atrium.

Furukawa¹,

Saegusa²,

Ogiwara³

et al. 1988

Jpn.J.Physiol

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Effects of physostigmine and of beating rate on the negative chronotropic and inotropic responses to tonic intramural parasympathetic nerve stimulation at a frequency of 5 Hz for 2 min were investigated, using the isolated, blood-perfused dog atrium which was pretreated with propranolol. The responses to stimulation reached a maximum, and then "faded" back toward the control levels during stimulation . Before physostigmine, the fade of the inotropic response was consistently observed but the fade of the chronotropic response was minimal. Both the maximum effect and the fade of the chronotropic response were augmented dosedependently by physostigmine in spontaneously beating atria. Physostigmine increased the maximum chronotropic response to infusion of acetylcholine (ACh) but did not potentiate the fade response. These results suggest that the potentiation of the fade of the chronotropic response to stimulation after physostigmine is due to decreases in the amount of ACh at the neuroeffector junction. The maximum negative inotropic responses were dose-dependently potentiated similarly by physostigmine in isolated spontaneously beating or paced atria. The fade of the inotropic response in spontaneously beating atria was decreased along with reduction of the rate by physostigmine, whereas the fades in paced atria at 2 and 3 Hz were not changed, showing that decreases in rate during stimulation influenced the reduction of the fade. Increases in contractile force induced by infusion of CaC12 did not alter the maximum and fade responses to stimulation in 2 Hz paced atria. The blood flow into an isolated atrium was not changed detectably during stimulation. These results suggest that the fade of the inotropic response to parasympathetic nerve stimulation is related subsidiarily to acetylcholinesterase or washout of ACh at the neuroeffector junction in isolated perfused atria.

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The action of acetylcholine on background conductance in frog atrial trabeculae.

Cited by 90 publications

References 31 publications

Characterization of the acetylcholine‐induced potassium current in rabbit cardiac Purkinje fibres.

Characterization of the acetylcholine‐induced potassium current in rabbit cardiac Purkinje fibres.

Changes by acetylcholine of membrane currents in rabbit cardiac Purkinje fibres.

Fade responses at neuroeffector junction to vagal stimulation in the isolated, blood-perfused dog atrium.

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