Effects of external cadmium ions on excitation-contraction coupling in rat soleus fibres

Mould, Jeremy; Dulhunty, Angela F.

doi:10.1007/s004240050769

Cited by 10 publications

(19 citation statements)

References 25 publications

(41 reference statements)

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“…It is well known that Ca 2+ -induced Ca 2+ release is essential for normal function of excitation-contraction (e-c) coupling of cardiac muscle cells [20]. Several mechanisms are known to be involved in the modulation of e-c coupling [21]. Obviously, Zn 2+ -induced inhibition of Ca 2+ release from the SR found in this study is a novel way.…”

Section: Discussionmentioning

confidence: 65%

Inhibition of Ryanodine Binding to Sarcoplasmic Reticulum Vesicles of Cardiac Muscle by Zn<sup>2+</sup> Ions

Wang¹,

Wei²,

Cheng³

et al. 2001

Cell Physiol Biochem

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Using the assay of [³H]ryanodine binding to the sarcoplasmic reticulum, the effect of Zn²⁺ on ryanodine receptors (RyRs) of cardiac muscle was investigated. There was no obvious change in the binding at [Zn²⁺]_f of less than 0.2 µM. However, a decrease of the binding became significant with raising [Zn²⁺]_f to 0.5 µM. The inhibitory effect of Zn²⁺ was [Zn²⁺]_f-dependent, with IC_50/ZnI of 2.1±0.4 µM (mean±S.D.). Scatchard analysis indicates that both an increase of K_d and a decrease of B_max were responsible for Zn²⁺-induced decrease of the binding. The Hill coefficient for this inhibitory effect of Zn²⁺ was between 0.8 and 1.2. The interactions of the effects of Zn²⁺ and various modulators of RyR indicate that the inhibitory effect of Zn²⁺ was mostly mediated through inhibiting Ca²⁺ activation sites (CaA) on RyR. Since the [Zn²⁺]_f dependence was not clearly changed by [Ca²⁺]_f, the inhibitory effect of Zn²⁺ may not be due to competition of Zn²⁺ with Ca²⁺ for CaA and probably is indirect. The inhibitory effect of Zn²⁺ could not be antagonized by 2 mM dithiothreitol, a thiol-reducing agent, suggesting that the binding of Zn²⁺ ions to RyRs of cardiac muscle is not accompanied by obvious change of redox state of the RyRs. In comparison with that seen in skeletal muscle [3], the effects of Zn²⁺ on ryanodine binding to the sarcoplasmic reticulum of cardiac muscle show several distinct differences. It is indicated that the effect of Zn²⁺ on RyRs may be isoform-dependent. The physiological significance of the effects of Zn²⁺ is discussed.

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Section: Discussionmentioning

confidence: 65%

Inhibition of Ryanodine Binding to Sarcoplasmic Reticulum Vesicles of Cardiac Muscle by Zn<sup>2+</sup> Ions

Wang¹,

Wei²,

Cheng³

et al. 2001

Cell Physiol Biochem

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“…Peak tension (1) varied from 20% to 60% of control tetanic tension (Tc) and (2) was not related to the size of the rise in baseline tension (i.e. the Cd 2+ -induced contracture [18]) or the reduction in twitch and tetanic tension, during exposure to Cd 2+ (Fig. 1A,B).…”

Section: Characteristics Of the CD 2+ Withdrawal Contracturesmentioning

confidence: 89%

“…The solutions, and sequence of solution changes, are the same as in Mould and Dulhunty [18,19]. Cl -was the major anion in most experiments.…”

Section: Solution Compositionmentioning

confidence: 91%

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Cadmium withdrawal contractures in rat soleus muscle fibres

Mould

Dulhunty

2000

Pflugers Arch - Eur J Physiol

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Transient "Cd2+ withdrawal" contractures, with amplitudes of < or =60% peak tetanic tension, were seen when > or =3 mM Cd2+ was removed, after exposures lasting > or =5 min, from solutions bathing rat soleus fibres at 22 degrees C with Cl- as the major external anion. The minimum free [Cd2+] for withdrawal contractures was reduced twofold when the external anion was SO4(2-). Withdrawal contractures were not seen after removal of 3 mM Co2+, Zn2+ or La3+ and were not observed in rat extensor digitorum longus fibres. The contractures were not due to depolarization (membrane potential, Vm, did not change during Cd2+ removal) or to an influx of external Ca2+ (the transient tension increase was recorded when solutions either lacked Ca2+, or contained 2 mM Co2+). Cd2+ withdrawal contractures were abolished by inactivation of excitation-contraction coupling (ECC) following depolarization in 40 mM K+ for 20 min, and recovered from inactivation at the same time as twitch and tetanic contractions with repriming of ECC. Withdrawal contractures were depressed by agents that depress ECC, i.e. low [Ca2+], 2 mM Co2+, 30 mM Ca2+, 30 mM Mg2+ and 50 microM nifedipine. The results support a hypothesis in which withdrawing Cd2+ from the external solution induces a contracture by activating the voltage sensor for ECC.

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“…Several effects of Zn 2+ on the function of both smooth muscle and skeletal muscle have been described: inhibition of Ca-ATPase of the sarcoplasmic 120 Cheng/Chen/Zhang/Zhu reticulum (SR) [2], depression of Ca 2+ release from the SR [3], alteration of excitation-contraction coupling [4], induction of delayed contracture [5] etc.…”

Section: Introductionmentioning

confidence: 99%

Effect of Zinc Ions on Caffeine-Induced Contracture in Vascular Smooth Muscle and Skeletal Mu-scle of Rat

Cheng¹,

Chen²,

Zhang³

et al. 2002

Cell Physiol Biochem

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The effect of zinc ions on caffeine-induced contracture in vascular smooth muscle and skeletal muscle of rat was studied. In aortic strips, caffeine contracture was depressed by Zn²⁺ in a dose-dependent manner. Moreover, the extent of the depression of caffeine contracture in the Zn²⁺ loaded smooth muscle increased with repetitive caffeine exposures. For instance, in the preparations perfused with a medium containing 100 µM [Zn²⁺] for 15 or 30 min, the first caffeine contractures were similarly depressed to about 60% of the control. However, the subsequent caffeine exposure at 15 min interval could not evoke any contracture. In this study this feature is referred to as activation dependence of the Zn²⁺ effect. In small bundles of soleus muscle 2∼100 µM [Zn²⁺] similarly caused a depression of caffeine contracture, and the activation dependence also was evident. However, an evident potentiation of caffeine contracture was seen in the preparations loaded with lower [Zn²⁺] such as 0.5 µM, indicating that the effect of Zn²⁺ on caffeine contracture of skeletal muscle was somewhat different from that seen in smooth muscle. By observing how the depression effect depends on the intervals between caffeine exposures as well as on caffeine concentrations, it is indicated that the activation dependence of the Zn²⁺ effect, at least in skeletal muscle, may not be explained by depletion of intracellular Ca²⁺ stores alone. The possible mechanism for that caffeine contracture of smooth muscle and skeletal muscle was differentially affected by Zn²⁺ ions is discussed.

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Effects of external cadmium ions on excitation-contraction coupling in rat soleus fibres

Cited by 10 publications

References 25 publications

Inhibition of Ryanodine Binding to Sarcoplasmic Reticulum Vesicles of Cardiac Muscle by Zn<sup>2+</sup> Ions

Inhibition of Ryanodine Binding to Sarcoplasmic Reticulum Vesicles of Cardiac Muscle by Zn<sup>2+</sup> Ions

Cadmium withdrawal contractures in rat soleus muscle fibres

Effect of Zinc Ions on Caffeine-Induced Contracture in Vascular Smooth Muscle and Skeletal Mu-scle of Rat

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