Abstract <p>We previously demonstrated that fragments of the central loop of the non-conventional toxin WTX reduce blood pressure in rats and inhibit certain nicotinic acetylcholine receptor subtypes [10]. In the present study, we examined the effects of hexamethonium and methylicaconitine, which are nicotinic acetylcholine receptor inhibitors, as well as of atropine, a muscarinic acetylcholine receptor inhibitor, on the hypotensive effect of the WTX central loop fragment. For this purpose, these compounds were administered intravenously before the peptide. We found that hexamethonium and methylicaconitine enhanced the fragment’s hypotensive effect, while atropine weakened this effect. Only methylicaconitine enhanced the tachycardic effect of the peptide. These data indicate the involvement of both nicotinic and muscarinic acetylcholine receptors in the hemodynamic effects of the WTX central loop fragment.</p>

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Blockers of Acetylcholine Receptors Affect the Hypotensive Effect of the Central Loop Fragment of the WTX Toxin

  • M. S. Severyukhina,
  • A. M. Ismailova,
  • E. R. Shaykhutdinova,
  • N. S. Egorova,
  • I. A. Dyachenko,
  • V. I. Tsetlin,
  • Yu. N. Utkin

摘要

Abstract

We previously demonstrated that fragments of the central loop of the non-conventional toxin WTX reduce blood pressure in rats and inhibit certain nicotinic acetylcholine receptor subtypes [10]. In the present study, we examined the effects of hexamethonium and methylicaconitine, which are nicotinic acetylcholine receptor inhibitors, as well as of atropine, a muscarinic acetylcholine receptor inhibitor, on the hypotensive effect of the WTX central loop fragment. For this purpose, these compounds were administered intravenously before the peptide. We found that hexamethonium and methylicaconitine enhanced the fragment’s hypotensive effect, while atropine weakened this effect. Only methylicaconitine enhanced the tachycardic effect of the peptide. These data indicate the involvement of both nicotinic and muscarinic acetylcholine receptors in the hemodynamic effects of the WTX central loop fragment.