Mode of stimulatory actions of cadmium ion on the mouse diaphragm

Fu, Wen‐Mei; Lin‐Shiau, Shoei‐Yn

doi:10.1111/j.1476-5381.1985.tb08884.x

Cited by 6 publications

(3 citation statements)

References 22 publications

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“…By the use of conventional microelectrodes, it was found that Cd +2 not only depolarized the muscle membrane, but also induced spontaneous action potentials at a high frequency (Fu and Lin-Shiau 1985). It was reported that increased Na + permeability of the muscle membrane was the essential step bringing about spontaneous contractions.…”

Section: Discussionmentioning

confidence: 99%

“…Studies on the phrenic nerve-diaphragm preparation of the mouse showed that Cd +2 increased the contractions (Fu and Lin-Shiau 1985). By the use of conventional microelectrodes, it was found that Cd +2 not only depolarized the muscle membrane, but also induced spontaneous action potentials at a high frequency (Fu and Lin-Shiau 1985).…”

Section: Discussionmentioning

confidence: 99%

“…It was reported that increased Na + permeability of the muscle membrane was the essential step bringing about spontaneous contractions. The binding of Cd +2 to thiol groups of the membrane was closely related to the induction of these effects (Fu and Lin-Shiau 1985).…”

Section: Discussionmentioning

confidence: 99%

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Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Ozturk

Büyükakıllı

Ballı

et al. 2009

Toxicology Mechanisms and Methods

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In this study, the systemic hemodynamics induced by acute and chronic cadmium (Cd+2) intoxication in the cardiovascular system of rats using thoracic electrical bioimpedance were examined and the acute and chronic effects of Cd+2 intoxication on the activities of antioxidant enzymes and malondialdehyde (MDA) were compared. Also, in this study, ultrastructural changes in the heart and aorta of rats were evaluated. Thirty-eight male Wistar albino rats were randomly divided into control, acute, and chronic groups. Chronic group was administered by oral gavage an aqueous solution of CdCl2 for 60 days, at dose of 15 mg Cd+2/kg/day. Acute group was administered by oral gavage an aqueous solution of CdCl2 with a single dose of 15 mg Cd+2/kg. Cadmium increased the stroke volume and cardiac output of rats in the chronic group, but did not change the heart rate significantly. Antioxidant enzymes activities and MDA level significantly increased in the chronic group. In ultrastructural examination, there were widespread degenerative changes in heart muscle cells of the chronic group but endothelial cells and smooth muscle cells in the aorta tissue samples had normal morphological features in all groups. All of the findings indicate that Cd+2 toxication can cause deformation in heart muscle cells due to an increase in free radicals and lipid peroxidation. Also, this study has confirmed that a long-term-Cd+2 exposure increased stroke volume (SV) and cardiac output (CO), but did not change the heart rate (HR).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Ozturk

Büyükakıllı

Ballı

et al. 2009

Toxicology Mechanisms and Methods

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Studies on cadmium-induced myotonia in the mouse diaphragm

Day

Lin‐Shiau

1989

Naunyn-Schmiedeberg's Arch Pharmacol

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The purpose of this investigation was to study the possible mechanism of the potentiation of the contractile response and myotonia caused by Cd2+ in the mouse diaphragm. Cd2+ increased both amplitude and duration of the contractile response to direct stimulation in either 0.25 mM Ca2+ Krebs or 2.5 mM Ca2+ Krebs containing the K+-channel blockers, 4-aminopyridine, uranyl nitrate or tetraethylammonium ion. High K+ and tetrodotoxin inhibited these effects of Cd2+. Electrophysiological studies revealed that only one or two action potentials were triggered by passing a short depolarizing current across the muscle fibre membrane in 0.25 mM Ca2+ Krebs, but in the presence of Cd2+, a train of action potentials (153 +/- 21 Hz) which lasted for 0.7 +/- 0.2 s was induced. Furthermore, Cd2+ triggered a train of action potentials evoked by a single extracellular direct stimulation on the muscle fibre in 2.5 mM Ca2+ Krebs solution containing either 4-aminopyridine or uranyl nitrate. The membrane depolarized during the repetitive firing and then repolarized immediately after the cessation of repetitive firing. Cd2+ (0.1 mM) increased the input resistance of the muscle fibre by 53 +/- 7% and this effect was inhibited in low [Cl-]o. These findings suggest that the contractile potentiation and myotonia induced by Cd2+ in the mouse diaphragm are mediated by lowering the Cl- conductance of the membrane.

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Use of ion channel blockers in the exploration of possible mechanisms involved in the myopathy of diabetic mice

Lin‐Shiau

Liu

Lin

1993

Naunyn-Schmiedeberg's Arch Pharmacol

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Changes in the muscle contractions of the phrenic nerve-diaphragm preparation from the diabetic mouse were investigated by means of K(+)- and Cl(-)-channel blockers and the Ca(2+)-mobilizing agent, selenite. The K(+)-channel blockers (UO2(2+) and 4-aminopyridine) cooperated synergistically with the Cl(-)-channel blockers (Cd2+ and 9-anthracenecarboxylic acid) in increasing normal muscle contraction as described previously, but failed to induce this effect in the diaphragm of the diabetic mouse. Treatment with a Cl(-)-channel blocker alone in 0.25 mmol/l Ca2+ Krebs solution induced a myotonic activity accompanied by stimulus-bound repetitive action potential firings. This effect was also diminished in the diaphragm from diabetic mice. The membrane potential of the muscle cells in the diaphragm of the diabetic mouse was slightly but significantly decreased. The membrane input resistance was also increased and was refractory to being further increased by either a Cl(-)-channel blocker or a low Cl(-)-medium. Furthermore, the membrane chloride conductance was found to be decreased, but the membrane K+ conductance remained unchanged in the muscle from diabetic mice. These changes of membrane properties in the muscles from diabetic mice were shown to be similar to those induced by either Cl(-)-channel blockers or a low Cl(-)-medium. In addition, the combined treatment of the diaphragm from diabetic mice with Cd2+ plus UO2(2+) in 0.25 mmol/l Ca2+ Krebs solution and then stepwise replenishment of Ca2+ led to a greater restoration of muscle contractions at a lower cumulative Ca2+ concentration than that was found with the normal diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)

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Mode of stimulatory actions of cadmium ion on the mouse diaphragm

Cited by 6 publications

References 22 publications

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

Studies on cadmium-induced myotonia in the mouse diaphragm

Use of ion channel blockers in the exploration of possible mechanisms involved in the myopathy of diabetic mice

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