Myotonia as a Side Effect of Diuretic Action

Bretag, Allan H.; Dawe, S. R.; Kerr, Donald; Moskwa, Anna

doi:10.1111/j.1476-5381.1980.tb10959.x

Cited by 22 publications

(9 citation statements)

References 26 publications

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“…Although frusemide has been reported to inhibit Pc1 (e.g. Bretag, Dawe, Kerr & Moskwa, 1980) which would contribute to the hyperpolarization, this was at a much higher concentration than used in the present study (2-5 mm cf. 10 ,tM).…”

Section: Effect Offrusemidementioning

confidence: 69%

Intracellular chloride and the mechanism for its accumulation in rat lumbrical muscle.

Aickin

Betz

Harris

1989

The Journal of Physiology

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SUMMARY1. Double-barrelled Cl--sensitive microelectrodes have been used to measure the intracellular Cl-activity (a',) and membrane potential (Em) in rat lumbrical muscles. The mean Cl-equilibrium potential (Ecl), calculated from the measured aC1 in sixty fibres, was 29 + 25 mV (S.D. of an observation) less negative than Em. The value of a', was higher than would be expected for a passive distribution, by a mean 1P4 + 1 2 mm. The mean Em was -59-5 + 8-2 mV. 3. If lack of selectivity of the Cl--sensitive ion exchanger and the intracellular presence of interfering anions, assumed to be responsible for the apparent al1 recorded in Cl--depleted fibres, were also responsible for the apparently non-passive Cl-distribution recorded under normal conditions, the difference between the calculated EC1 and Em would increase at more negative potentials. This was not observed over a range of Em values between -46 and -84 mV. 4. Inhibition of the Cl-permeability by application of 9-anthracene carboxylic acid (9-AC) resulted in an immediate rise in ai1 and hyperpolarization. An ai1 up to 40 mm higher, or eleven times higher, than that predicted by a passive distribution was recorded. Application of 9-AC after depletion of intracellular Cl-in Cl--free solution had no effect on either the apparent ai1 or Em.5. It is concluded that Cl-ions are actively accumulated by the skeletal muscle fibre and that the Cl-distribution therefore normally exerts a depolarizing influence.6. In the presence of 9-AC and nominal absence of CO2 and HC03-, readdition of Cl-to Cl--depleted fibres resulted in a substantial rise in a', and a small, maintained 7. Neither application of CO2 and HCQ3-nor application of DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid) had any effect on the accumulation of Cl-ions. This suggests that Cl--HC03-exchange is not involved.8. Removal of Na+ or K+ resulted in a limited rise in a'1 such that EC1 approximated to Em. Removal of both cations had no greater effect than the absence of only one. Readdition of the cations caused an immediate accumulation of Cl-ions and divergence of Ec1 from Em. This was largely inhibited by the presence of frusemide. These results suggest that a Na+, K+, Cl-co-transport mechanism is responsible for the inward transport of Cl-.

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Section: Effect Offrusemidementioning

confidence: 69%

Intracellular chloride and the mechanism for its accumulation in rat lumbrical muscle.

Aickin

Betz

Harris

1989

The Journal of Physiology

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“…7, A-C shows that both EA and FLX inhibited 36 Cl Ϫ efflux and cytosolic Ca 2ϩ elevation in a dose-dependent manner. Intriguingly, the calculated IC 50 Ϫ efflux may play a role in the mobilization of Ca 2ϩ from intracellular stores, neutrophils were preincubated with either EA or FLX in Ca 2ϩ -free, EGTAcontaining buffer and exposed to opsonized C. albicans particles. Fig.…”

Section: Relationship Between CLmentioning

confidence: 99%

Chloride Movements in Human Neutrophils during Phagocytosis: Characterization and Relationship to Granule Release

Busetto

Trevisan

Decleva

et al. 2007

The Journal of Immunology

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Chloride ion efflux is an early event occurring after exposure of human neutrophils to several soluble agonists. Under these circumstances, a rapid and reversible fall in the high basal intracellular chloride (Cl−i) levels is observed. This event is thought to play a crucial role in the modulation of several critical neutrophil responses including activation and up-regulation of adhesion molecules, cell attachment and spreading, cytoplasmic alkalinization, and activation of the respiratory burst. At present, however, no data are available on chloride ion movements during neutrophil phagocytosis. In this study, we provide evidence that phagocytosis of Candida albicans opsonized with either whole serum, complement-derived opsonins, or purified human IgG elicits an early and long-lasting Cl− efflux accompanied by a marked, irreversible loss of Cl−i. Simultaneous assessment of Cl− efflux and phagocytosis in cytochalasin D-treated neutrophils indicated that Cl− efflux occurs without particle ingestion. These results suggest that engagement of immune receptors is sufficient to promote chloride ion movements. Several structurally unrelated chloride channel blockers inhibited phagocytosis-induced Cl− efflux as well as the release of azurophilic—but not specific—granules. It implicates that different neutrophil secretory compartments display distinct sensitivity to Cl−i modifications. Intriguingly, inhibitors of Cl− exchange inhibited cytosolic Ca2+ elevation, whereas Cl− efflux was not impaired in Ca2+-depleted neutrophils. We also show that FcγR(s)- and CR3/CR1-mediated Cl− efflux appears to be dependent on protein tyrosine phosphorylation but independent of PI3K and phospholipase C activation.

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“…Loop diuretics, frusemide, ethacrynic acid and mersalyl have produced myotonia in vitro. It is feasible that the muscle cramps, tetanic spasms and weakness seen with these diuretics is a form of drug induced myotonia 37 .…”

Section: Agents Exacerbating Myotoniamentioning

confidence: 99%

Chemically induced or inherited myotonia?

Coyne

1993

Emergency Medicine

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Objective: To present a case of chemically induced myotonia occuring as a result of intentional ingestion of trifluoperazine and Defender Australia Bindi plus Clover Lawn WeederR (chlorophenoxy compounds present as 4‐chloro‐2‐methylphenoxyacetic acid (MCPA) as a dimethylamine salt 15% W/V and 3,6‐dichloro‐2‐methoxybenzoic acid (dicamba) 2.5% W/V). To discuss myotonia. Clinical features: A 38 year old man with features suggestive of dystrophia myotonica presented with severe myotonia, urinary retention and dry lips. There was no personal or known family history of this muscular disorder. Intervention: He was treated with 2mgs of intravenous benztropine mesylate, and 50 grams of activated charcoal and 150 mls of 70% sorbitol orally. An indwelling catheter was inserted. Laryngoscopy and upper gastrointestinal tract endoscopy were performed. The myotonia was managed conservatively and complete recovery occurred as evidenced by normal electromyography on day six of his admission. Conclusion: Myotonia is a rare complication of toxin ingestion. In this case, the toxins may have unmasked subclinical dystrophia myotonica or induced myotonia de novo.

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Myotonia as a Side Effect of Diuretic Action

Cited by 22 publications

References 26 publications

Intracellular chloride and the mechanism for its accumulation in rat lumbrical muscle.

Intracellular chloride and the mechanism for its accumulation in rat lumbrical muscle.

Chloride Movements in Human Neutrophils during Phagocytosis: Characterization and Relationship to Granule Release

Chemically induced or inherited myotonia?

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