ArticleBritish journal of pharmacology2007
Verrucotoxin, a stonefish venom, modulates calcium channel activity in guinea-pig ventricular myocytes.
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Proteomic Diversity of the Sea AnemoneMarine drugs · 2025Article
- Stingray Venom Proteins: Mechanisms of Action Revealed Using a Novel Network Pharmacology Approach.Marine drugs · 2021Article
- Fish Cytolysins in All Their Complexity.Toxins · 2021Review
- The Geographic Distribution, Venom Components, Pathology and Treatments of Stonefish (Marine drugs · 2021Review
- Article
- Transcriptomic Analysis of Four Cerianthid (Cnidaria, Ceriantharia) Venoms.Marine drugs · 2020Article
- Bioactive components in fish venoms.Toxins · 2015Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeStonefish (Synanceia genus) are commonly found in shallow waters of the Pacific and Indian Oceans. The venom of stonefish is stored in the dorsal fine spines and contains a proteinaceous toxin, verrucotoxin (VTX). The stings produced by the spines induce intense pain, respiratory weakness, damage to the cardiovascular system, convulsions and paralysis, sometimes leading to death. Although there are many studies on VTX, the mechanism(s) underlying the VTX-mediated cardiotoxicity is not yet fully understood. The aim of this study was to investigate the modulation of ion channels in cardiac tissue by VTX. EXPERIMENTAL APPROACH: The effects of VTX on changes in the voltage or current in guinea-pig ventricular myocytes were investigated using a patch clamp method. KEY
resultsVTX (10 microg ml(-1)) prolonged the action potential duration by 2.5-fold. VTX increased L-type Ca(2+) currents (I (Ca(L))) in a concentration-dependent manner with a EC(50) value of 7 microg ml(-1) and a maximum increase of 3.1-fold. The non-selective beta-adrenoceptor antagonist, propranolol (1 microM) and the selective beta(1)-adrenoceptor antagonist, CGP20712A (10 microM) each abolished the effect of VTX (100 microg ml(-1)) on I (Ca(L)). Furthermore, the protein kinase A (PKA) antagonists H-89 (10 microM) and Rp-8-Br-cAMPS (30 microM) inhibited the effect of VTX on I (Ca(L)). CONCLUSIONS AND IMPLICATIONS: VTX modulates Ca(2+) channel activity through the beta-adrenoceptor-cAMP-PKA pathway.
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