ArticleMarine drugs2013
Tetrodotoxin blockade on canine cardiac L-type Ca²⁺ channels depends on pH and redox potential.
Article in Marine drugs, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- Pufferfish exposure and presumed tetrodotoxicosis in Australian dogs: 372 cases (2007-2018).Australian veterinary journal · 2026Article
- A review of chemical defense in harlequin toads (Bufonidae:Toxicon: X · 2022Review
- Brugada Syndrome: Warning of a Systemic Condition?Frontiers in cardiovascular medicine · 2021Review
- Tetrodotoxin, an Extremely Potent Marine Neurotoxin: Distribution, Toxicity, Origin and Therapeutical Uses.Marine drugs · 2015Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tetrodotoxin (TTX) is believed to be one of the most selective inhibitors of voltage-gated fast Na⁺ channels in excitable tissues. Recently, however, TTX has been shown to block L-type Ca²⁺ current (I(Ca)) in canine cardiac cells. In the present study, the TTX-sensitivity of I(Ca) was studied in isolated canine ventricular myocytes as a function of (1) channel phosphorylation, (2) extracellular pH and (3) the redox potential of the bathing medium using the whole cell voltage clamp technique. Fifty-five micromoles of TTX (IC₅₀ value obtained under physiological conditions) caused 60% ± 2% inhibition of I(Ca) in acidic (pH = 6.4), while only a 26% ± 2% block in alkaline (pH = 8.4) milieu. Similarly, the same concentration of TTX induced 62% ± 6% suppression of ICa in a reductant milieu (containing glutathione + ascorbic acid + dithiothreitol, 1 mM each), in contrast to the 31% ± 3% blockade obtained in the presence of a strong oxidant (100 μM H₂O₂). Phosphorylation of the channel protein (induced by 3 μM forskolin) failed to modify the inhibiting potency of TTX; an IC₅₀ value of 50 ± 4 μM was found in forskolin. The results are in a good accordance with the predictions of our model, indicating that TTX binds, in fact, to the selectivity filter of cardiac L-type Ca channels.
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