Anion channels activated by adrenaline in cardiac myocytes

Ehara, Tsuguhisa; Ishihara, Keiko

doi:10.1038/347284a0

Cited by 89 publications

(46 citation statements)

References 25 publications

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“…The observed hyperpolarization of the membrane potential, V., by isoprenaline in skeletal muscle fibres, has been attributed to stimulation of the Na+-K+-pump by the cyclic AMPdependent cascade (Clausen, 1986;Li & Sperelakis, 1993). From the literature on cardiac tissue however, a more complex picture emerges comprising influences on V. by the stimulation of the Na+-K+-pump (D1silets & Baumgarten, 1986), K+-conductance (Gadsby, 1983;Boyden et al, 1983a), Na+-conductance (Egan et al, 1988), Ca2+-conductance (Tsien et al, 1986) or Cl--conductance (Harvey & Hume, 1989;Ehara & Ishihara, 1990;Nakaya et al, 1990). Also combinations of these effects have been proposed (Encina et al, 1988;Harvey et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Modulation of the isoprenaline‐induced membrane hyperpolarization of mouse skeletal muscle cells

Mil

Kerkhof

Heukelom

1995

British J Pharmacology

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1 The hyperpolarization of the resting membrane potential, V., induced by isoprenaline in the lumbrical muscle fibres of the mouse, was investigated by use of intracellular microelectrodes.2 In normal Krebs-Henseleit solution (potassium concentration: K+= 5.7 mM, 'control'), V. was -74.0±0.2 mV; lowering K+ to 0.76 mM ('low K'7) resulted in either a hyperpolarization (VM -95.7± 2.9 mV), or a depolarization (Vm= -52.0± 0.3 mV). When Vm hyperpolarized after switching to low K', the addition of isoprenaline resulted in increased hyperpolarization Vm: AVm=-16.3 + 3.2 mV to a final Vm=-110.1I±3.4 mV. Adding iso-prenaline when Vm depolarized in low K+, leads to a hyperpolarization of either by -11.6 ± 0.5 mV to -63.6+0.8 mV or by -51.7+2.7 mV to -106.9±3.9 mV. 5 Ouabain (0.1 to 1 mM) did not suppress the hyperpolarization by isoprenaline in 5.7 mM K + (AVm=-6.7±0.4 mV) or the hyperpolarization of the depolarized cells in low K + (AVm= 9.7 ±1.5 mV). 6The hyperpolarization is a logarithmically decreasing function of K + in the range between 2 and 20 mM (12 mV/decade). 7 IBMX and 8Br-cyclic AMP mimicked the response to isoprenaline whereas forskolin (FSK) induced in low K + a hyperpolarization of -7.0±0.7 mV that could be augmented by addition of isoprenaline (AVm -8.2± 1.8 mV). 8In control and low K+, Ba2`(0.6 mM) inhibited the hyperpolarization induced by isoprenaline, IBMX or 8Br-cyclic AMP. Other blockers of the potassium conductance such as TEA (5 mM) and apamin (0.4 riM) had no effect. 9 We conclude that in the lumbrical muscle of the mouse the isoprenaline-induced hyperpolarization is primarily due to an increase in potassium permeability.

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Section: Introductionmentioning

confidence: 99%

Modulation of the isoprenaline‐induced membrane hyperpolarization of mouse skeletal muscle cells

Mil

Kerkhof

Heukelom

1995

British J Pharmacology

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“…Recently, it has been suggested that the cystic fibrosis transmembrane regulator protein (CVlrR) is a CI-channel which is regulated by intracellular cAMP (Rich, Gregory, Anderson, Manavalin, Smith, and Welsh, 1991;Bear, Duguay, Naismith, Kartner, Hanratian, and Riordan, 1991;Anderson, Gregory, Thompson, Souza, Paul, Mulligan, Smith, and Welsh, 1991). In addition, a cardiac CI-channel that is activated by 13-adrenergic agonists (Harvey and Hume, 1989;Bahinski, Nairn, Greengard, and Gadsby, 1989;Ehara and Ishihara, 1990;Matsuoka, Ehara, and Noma, 1990) may well be the product of a cardiac CFTR gene (Levesque, Hart, Hume, Kenyon, and Horowitz, 1992). This and other cardiac CI-currents and channels have been recently reviewed (Ackerman and Clapham, 1993).…”

Section: Comparison With Other Chloride Currentsmentioning

confidence: 99%

Hyperpolarization-activated chloride currents in Xenopus oocytes.

Kowdley

Ackerman

John

et al. 1994

The Journal of General Physiology

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During hyperpolarizing pulses, defolliculated Xenopus oocytes have time-and voltage-dependent inward chloride currents. The currents vary greatly in amplitude from batch to batch; activate slowly and, in general, do not decay; have a selectivity sequence of I-> NO~ > Br-> C1-> propionate > acetate; are insensitive to Ca 2+ and pH; are blocked by Ba 2+ and some chloride channel blockers; and have a gating valence of ~ 1.3 charges. In contrast to hyperpolarization-activated chloride currents induced after expression of phospholemman (Palmer, C.

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“…Catecholamines also increase the background conductances of cardiac muscle (Gadsby, 1983; Eagan, Noble, Noble, Powell, Twist & Yamaoka, 1988;Bahinski, Nairn, Greengard & Gadsby, 1989;Harvey & Hume, 1989;Matsuoka, Ehara & Noma, 1990). Recently a Cl-channel was identified on the single-channel level, underlying the catecholamine-induced conductance (Ehara & Ishihara, 1990).…”

Section: Introductionmentioning

confidence: 99%

Beta‐adrenergic and muscarinic regulation of the chloride current in guinea‐pig ventricular cells.

Tareen

Ono

Noma

et al. 1991

The Journal of Physiology

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SUMMARY1. Single guinea-pig ventricular cells were voltage clamped using the patch clamp method combined with the pipette-perfusion technique. The voltage-dependent current systems were mostly blocked, and the background membrane conductance was measured by applying ramp pulses.2. fl-Adrenergic effectors and related substances such as adrenaline, isoprenaline, forskolin or internal application of cyclic AMP induced a current component which showed a reversal potential near the expected Cl-equilibrium potential as well as an outward rectification in the I-V relation. It is suggested that the activation of this Cl-current was due to phosphorylation of the channel protein or related structure by the cyclic AMP-dependent protein kinase. Coincidentally with the activation of the Cl-current, the membrane capacitance of the cell decreased reversibly.3. Acetylcholine (ACh) depressed the responses induced by ,?-adrenergic stimulation and forskolin, but failed to interfere with the one induced by cyclic AMP.4. The dose dependence of the Cl-current activation by isoprenaline or forskolin was fitted by the Hill equation, with a coefficient of 1-9 and a half-maximum concentration Ki = 13 nm for isoprenaline, and with a Hill coefficient of 3 and a K1 = 1-2 /tM for forskolin. In the presence of 5.5 ,tM-ACh the dose-response relation shifted to higher doses; K1 was 65 nm for isoprenaline and 3-6 ,UM for forskolin.5. Washing out ACh in the presence of isoprenaline frequently caused transient overshoots of the response. When a saturating concentration of isoprenaline was used, this rebound was not observed.6. The internal application of cyclic GMP enhanced the response of the Cl-current induced by isoprenaline or adrenaline.7. When cyclic AMP was applied internally, the response was small in most cells.When the cell was superfused with 20 Itm-IBMX (3-isobutyl-1-methylxanthine), the Cl-current was consistently induced by the application of cyclic AMP. It is suggested that phosphodiesterase activity strongly buffered the influx of cyclic AMP through the patch pipette tip. 8. We suggest that the compensatory interaction between the ,-adrenergic

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Anion channels activated by adrenaline in cardiac myocytes

Cited by 89 publications

References 25 publications

Modulation of the isoprenaline‐induced membrane hyperpolarization of mouse skeletal muscle cells

Modulation of the isoprenaline‐induced membrane hyperpolarization of mouse skeletal muscle cells

Hyperpolarization-activated chloride currents in Xenopus oocytes.

Beta‐adrenergic and muscarinic regulation of the chloride current in guinea‐pig ventricular cells.

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