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Effects of goniopora toxin on bullfrog atrial muscle are frequency-dependent

  • Mami Noda
  • Ikunobu Muramatsu
  • Motohatsu Fujiwara
  • Katsuro Ashida
Article

Summary

When goniopora toxin (GPT), a marine toxin isolated from coral, was applied to the bullfrog atrial muscle, the duration of action potential (APD) was prolonged, and a positive inotropic effect was produced. Such effects of GPT were influenced by stimulus frequency. At lower frequencies of 0.1 Hz, GPT (10 to 100 nmol/l) produced a moderate prolongation of APD and positive inotropic effect. At higher prequencies (1.0 Hz), however, the effects of GPT on both APD and contraction were suppressed. In contrast, APD and duration of contraction were prolonged with long intervals of stimulation (1–3 min), in the presence of GPT. The rested-state contraction was also markedly increased and prolonged by GPT. When the membrane potential was conditioned by voltage clamp pulses, the prolonged action potential in GPT-treated muscle was shortened in proportion to the increase in conditioning depolarization. However, the shortening effect of conditioning depolarization was attenuated by lengthening the resting period after the conditioning depolarization. These results, in conjunction with our previous results, suggest that the frequency-dependent effects of GPT on APD and contraction reflect time-and membrane potential-dependent changes of the toxin-modified sodium channels.

Key words

Goniopora toxin Frog atria Sodium channel Action potential duration Positive inotropic effect 

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References

  1. Attwell D, Cohen I, Eisner DA (1981) The effects of heart rate on the action potentials of guinea-pig and human ventricular muscle. J Physiol (Lond) 313:439–461Google Scholar
  2. Beress L, Ritter R, Ravens U (1982) The influence of the rate of electrical stimulation on the effects of theAnemonia sulcata toxin ATX II in guinea pig papillary muscle. Eur J Pharmacol 79:265–272Google Scholar
  3. Carmeliet E (1977) Repolarization and frequency in cardiac cells. J Physiol (Paris) 73:903–923Google Scholar
  4. Catterall WA (1977) Membrane potential-dependent binding of scorpion toxin to the action potential Na ionophore. J Biol Chemistry 252:8660–8668Google Scholar
  5. Catterall WA (1979) Binding of scorption toxin to receptor sites associated with sodium channels in frog muscle. J Gen Physiol 74:375–391Google Scholar
  6. Catterall WA (1980) Neurotoxins that act on voltage-sensitive sodium channels in excitable membranes. Ann Rev Pharmacol Toxicol 20:15–44Google Scholar
  7. Fujiwara M, Muramatsu I, Hidaka H, Ikushima S, Ashida K (1979) Effects of goniopora toxin, a polypeptide isolated from coral, on electromechanical properties of rabbit myocardium. J Pharmacol Exp Ther 210:153–157Google Scholar
  8. Hashimoto Y, Ashida K (1973) Screening of toxic corals and isolation of a toxic polypeptide fromGoniopora spp. In: Proceedings of the Second International Symposium on Cnidaria. Publ Seto Mar Biol Lab 20:703–711Google Scholar
  9. Honerjäger P (1982) Cardioactive substances that prolong the open state of sodium channels. Rev Physiol Biochem Pharmacol 92:1–74Google Scholar
  10. Honerjäger P, Reiter M (1975) The relation between the effects of veratridine on action potential and contraction in mammalian ventricular myocardium. Naunyn-Schmiedeberg's Arch Pharmacol 289:1–28Google Scholar
  11. Hume JR, Giles W (1983) Ionic currents in single isolated bullforg atrial cells. J Gen Physiol 81:153–194Google Scholar
  12. Ikushima S, Muramatsu I, Fujiwara M, Ashida K (1981) Relationship between the effects of goniopora toxin on action potential and on contractile force in guinea-pig papillary muscle. Jpn J Pharmacol 31:1051–1060Google Scholar
  13. Isenberg G (1982) Ca entry and contraction as studied in isolated bovine ventricular myocytes. Z Naturforsch 37c:502–512Google Scholar
  14. Katzung BG (1982) Myocardial toxicity as the result of altered membrane channel function. In: Van Stee EW (ed) Cardiovascular toxicology. Raven Press, New York, pp 135–179Google Scholar
  15. Kodama I, Shibata S, Toyama J, Yamada K (1981) Electromechanical effects of anthopleurin-A (AP-A) on rabbit ventricular muscle: influence of driving frequency, calcium antagonist, tetrodotoxin, lidocaine and ryanodine. Br J Pharmacol 74:29–37Google Scholar
  16. Lazdunski M, Renaud JF (1982) The action of cardiotoxins on cardiac plasma membranes. Ann Rev Physiol 44:463–473Google Scholar
  17. Muramatsu I, Fujiwara M, Miura A, Narahashi T (1981) Effects of goniopora toxin, a polypeptide isolated from coral, on crayfish giant axon. Eighth International Congress of Pharmacology, Tokyo, p 318 (Abstract)Google Scholar
  18. Noda M, Muramatsu I, Fujiwara M (1984) Effects of goniopora toxin on the membrane currents of bullfrog atrial muscle. Naunyn-Schmiedeberg's Arch Pharmacol 327:75–80Google Scholar
  19. Vassalle M (1970) Electrogenic suppression of automaticity in sheep and dog Purkinje fibers. Circ Res 27:361–377Google Scholar
  20. Vincent JP, Balerna M, Barhanin J, Fosset M, Lazdunski M (1980) Binding of sea anemone toxin to receptor sites associated with gating system of sodium channel in synaptic nerve endingsin vitro. Proc Natl Acad Sci USA 77:1646–1650Google Scholar
  21. Warashina A, Fujita S (1983) Effect of sea anemone toxins on the sodium inactivation process in crayfish axons. J Gen Physiol 81:305–323Google Scholar
  22. Warashima A, Fujita S, Satake M (1981) Potential-dependent effects of sea anemone toxins and scorpion venom on crayfish giant axon. Pflügers Arch 391:272–276Google Scholar

Copyright information

© Springer-Verlag 1985

Authors and Affiliations

  • Mami Noda
    • 1
  • Ikunobu Muramatsu
    • 1
  • Motohatsu Fujiwara
    • 2
  • Katsuro Ashida
    • 2
  1. 1.Department of PharmacologyFukui Medical SchoolFukuiJapan
  2. 2.Department of Pharmacology, Faculty of MedicineKyoto UniversityKyotoJapan

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