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Cardiovascular effects of Buthus martensii (Karsch) scorpion venom

R Wang1, P Moreau, A Deschamps

  • 1Département de Physiologie, Faculté de Médecine, Université de Montréal, Québec, Canada.

Insights

Buthus martensii (Karsch) scorpion venom significantly raises blood pressure and enhances cardiac and arterial contractions in rats. These cardiovascular effects appear mediated by altered InsP3 metabolism in cardiac cells, not intracellular calcium in vascular cells.

Area of Science:

  • Pharmacology
  • Toxicology
  • Cardiovascular Research

Background:

  • Buthus martensii (Karsch) (BMK) scorpion envenomation is a prevalent health issue in China.
  • BMK scorpion venom is utilized in traditional Chinese medicine.
  • Systematic investigation into the cardiovascular effects of BMK venom is lacking.

Purpose of the Study:

  • To systematically investigate the cardiovascular effects of Buthus martensii (Karsch) scorpion venom.
  • To elucidate the mechanisms underlying the venom's cardiovascular actions.

Main Methods:

  • Intravenous injection of BMK venom in conscious rats to assess blood pressure and heart rate.
  • In vitro studies using isolated atrial and arterial strips to evaluate contractile responses.
  • Analysis of intracellular calcium ([Ca2+]i) in cultured vascular cells and InsP3 metabolism in cardiac myocytes.

Main Results:

  • BMK venom caused a dose-dependent increase in blood pressure in rats, sustained for over 50 minutes.
  • Heart rate remained unchanged in conscious rats.
  • In vitro, BMK venom increased the force of contraction in atrial and arterial strips.
  • These effects were inhibited by alpha 1-adrenergic antagonists (prazosin and tolazoline).
  • BMK venom did not alter [Ca2+]i in vascular and endothelial cells but increased InsP3 metabolism in cardiac myocytes.

Conclusions:

  • BMK venom exerts significant cardiovascular effects, including hypertension and enhanced cardiac and vascular contractility.
  • The cardiovascular effects are likely mediated by an alteration in InsP3 metabolism within cardiac myocytes.
  • The mechanism does not involve changes in intracellular calcium concentrations in vascular smooth muscle and endothelial cells.

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