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Glibenclamide does not block arterial relaxation caused by vasoactive intestinal polypeptide
Y Hattori1, M Nagashima, Y Endo
1Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan.
European Journal of Pharmacology
|March 17, 1992
Summary
Vasoactive intestinal polypeptide (VIP) relaxes rabbit arteries via the endothelium. ATP-sensitive K+ channels are not involved in VIP-induced relaxation, regardless of the endothelium presence.
Area of Science:
- Vascular pharmacology
- Endocrinology
Background:
- Vasoactive intestinal polypeptide (VIP) is a peptide with known vasodilatory effects.
- The precise mechanisms of VIP-mediated arterial relaxation are not fully elucidated, particularly the role of ion channels.
Purpose of the Study:
- To investigate the role of ATP-sensitive K+ (KATP) channels in VIP-induced relaxation of rabbit mesenteric arteries.
- To determine whether the endothelium is required for VIP-mediated arterial relaxation.
Main Methods:
- Rabbit mesenteric arteries were preconstricted.
- Concentration-response curves for VIP were generated in the presence and absence of endothelium.
- The effects of methylene blue (a guanylate cyclase inhibitor) and glibenclamide (a KATP channel blocker) on VIP-induced relaxation were assessed.
Main Results:
- VIP induced concentration-dependent relaxation in arteries with intact endothelium.
- Endothelium removal or methylene blue significantly inhibited VIP-induced relaxation.
- Glibenclamide did not affect VIP-induced relaxation, even in endothelium-denuded arteries.
Conclusions:
- Endothelium-dependent relaxation is a major component of VIP's effect on rabbit mesenteric arteries.
- ATP-sensitive K+ channels do not mediate VIP-induced arterial relaxation, either dependently or independently of the endothelium.