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Glibenclamide-sensitive hypotension produced by helodermin assessed in the rat
N Horikawa1, K Kataha, N Watanabe
1Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka, Japan.
Biological & Pharmaceutical Bulletin
|January 9, 1999
Summary
Helodermin, a lizard venom peptide, lowers blood pressure in rats by activating ATP-sensitive potassium channels (K(ATP) channels), similar to vasoactive intestinal polypeptide (VIP). This effect is blocked by glibenclamide, suggesting K(ATP) channel involvement.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Biochemistry
Background:
- Helodermin is a peptide found in lizard venom.
- Vasoactive intestinal polypeptide (VIP) is a known hypotensive agent.
- ATP-sensitive potassium (K(ATP)) channels play roles in cardiovascular regulation.
Purpose of the Study:
- To investigate the effects of helodermin on rat arterial blood pressure and heart rate.
- To determine if helodermin-induced hypotension involves the activation of K(ATP) channels.
- To compare helodermin's cardiovascular effects with those of VIP.
Main Methods:
- Administered helodermin and VIP to rats and monitored blood pressure and heart rate.
- Used glibenclamide to assess the role of K(ATP) channels.
- Used oxyhemoglobin to investigate the involvement of nitric oxide.
Main Results:
- Helodermin induced dose-dependent hypotension, comparable in potency and duration to VIP.
- Glibenclamide significantly attenuated hypotension caused by both helodermin and VIP.
- Oxyhemoglobin did not affect helodermin-induced hypotension but shortened acetylcholine-induced hypotension.
Conclusions:
- Helodermin-induced hypotension is partly mediated by the activation of glibenclamide-sensitive K(ATP) channels in arterial smooth muscle.
- Endothelium-derived relaxing factor/nitric oxide does not appear to be a major factor in helodermin's hypotensive effects.