ArticlePflugers Archiv : European journal of physiology2012
Tetrodotoxin blocks L-type Ca2+ channels in canine ventricular cardiomyocytes.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Beneficial Effect of Calcium Treatment for Hyperkalemia Is Not Due to "Membrane Stabilization".Critical care medicine · 2024Article
- A review of chemical defense in harlequin toads (Bufonidae:Toxicon: X · 2022Review
- Balance Between Rapid Delayed Rectifier KCirculation. Arrhythmia and electrophysiology · 2020Article
- Regional differences in the expression of tetrodotoxin-sensitive inward CaChannels (Austin, Tex.) · 2019Article
- Review
- β-adrenergic regulation of late NaJournal of molecular and cellular cardiology · 2018Article
- Diagnosis and Treatment of Lower Motor Neuron Disease in Australian Dogs and Cats.Journal of veterinary medicine · 2018Review
- Basal late sodium current is a significant contributor to the duration of action potential of guinea pig ventricular myocytes.Physiological reports · 2017Article
- Ca(2+)-Currents in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes Effects of Two Different Culture Conditions.Frontiers in pharmacology · 2016Article
- Tetrodotoxin blockade on canine cardiac L-type Ca²⁺ channels depends on pH and redox potential.Marine drugs · 2013Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tetrodotoxin (TTX) is believed to be the most selective inhibitor of voltage-gated fast Na(+) channels in excitable tissues, including nerve, skeletal muscle, and heart, although TTX sensitivity of the latter is lower than the former by at least three orders of magnitude. In the present study, the TTX sensitivity of L-type Ca(2+) current (I (Ca)) was studied in isolated canine ventricular cells using conventional voltage clamp and action potential voltage clamp techniques. TTX was found to block I (Ca) in a reversible manner without altering inactivation kinetics of I (Ca). Fitting results to the Hill equation, an IC(50) value of 55 ± 2 μM was obtained with a Hill coefficient of unity (1.0 ± s0.04). The current was fully abolished by 1 μM nisoldipine, indicating that it was really I (Ca). Under action potential voltage clamp conditions, the TTX-sensitive current displayed the typical fingerprint of I (Ca), which was absent in the presence of nisoldipine. Stick-and-ball models for Cav1.2 and Nav1.5 channel proteins were constructed to explain the differences observed between action of TTX on cardiac I (Ca) and I (Na). This is the first report demonstrating TTX to interact with L-type calcium current in the heart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.