Role of BKCa channels in cephalic vasodilation induced by CGRP, NO and transcranial electrical stimulation in the rat

A. Gozalov; I. Jansen-Olesen; Dan Arne Klærke; J. Olesen

doi:10.1111/j.1468-2982.2007.01409.x

Role of BK_Ca channels in cephalic vasodilation induced by CGRP, NO and transcranial electrical stimulation in the rat

A. Gozalov, I. Jansen-Olesen, Dan Arne Klærke, J. Olesen

23 Citations (Scopus)

Abstract

Both calcitonin gene-related peptide (CGRP) and nitric oxide (NO) are potent vasodilators that have been shown to induce headache in migraine patients. Their antagonists are effective in the treatment of migraine attacks. In the present study, we hypothesize that vasodilation induced by the NO donor glyceryltrinitrate (GTN) or by CGRP is partially mediated via large conductance calcium-activated potassium (BK(Ca)) channels. The effects of the BK(Ca) channel selective inhibitor iberiotoxin on dural and pial vasodilation induced by CGRP, GTN and endogenously released CGRP by transcranial electrical stimulation (TES) were examined. Iberiotoxin significantly attenuated GTN-induced dural and pial artery dilation in vivo and in vitro, but had no effect on vasodilation induced by CGRP and TES. Our results show that GTN- but not CGRP-induced dural and pial vasodilation involves opening of BK(Ca) channels in rat.

Original language	English
Journal	Cephalalgia
Volume	27
Issue number	10
Pages (from-to)	1120-1127
Number of pages	8
ISSN	0333-1024
DOIs	https://doi.org/10.1111/j.1468-2982.2007.01409.x
Publication status	Published - 2007

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title = "Role of BKCa channels in cephalic vasodilation induced by CGRP, NO and transcranial electrical stimulation in the rat",

abstract = "Both calcitonin gene-related peptide (CGRP) and nitric oxide (NO) are potent vasodilators that have been shown to induce headache in migraine patients. Their antagonists are effective in the treatment of migraine attacks. In the present study, we hypothesize that vasodilation induced by the NO donor glyceryltrinitrate (GTN) or by CGRP is partially mediated via large conductance calcium-activated potassium (BK(Ca)) channels. The effects of the BK(Ca) channel selective inhibitor iberiotoxin on dural and pial vasodilation induced by CGRP, GTN and endogenously released CGRP by transcranial electrical stimulation (TES) were examined. Iberiotoxin significantly attenuated GTN-induced dural and pial artery dilation in vivo and in vitro, but had no effect on vasodilation induced by CGRP and TES. Our results show that GTN- but not CGRP-induced dural and pial vasodilation involves opening of BK(Ca) channels in rat.",

author = "A. Gozalov and I. Jansen-Olesen and Kl{\ae}rke, {Dan Arne} and J. Olesen",

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T1 - Role of BKCa channels in cephalic vasodilation induced by CGRP, NO and transcranial electrical stimulation in the rat

AU - Gozalov, A.

AU - Jansen-Olesen, I.

AU - Klærke, Dan Arne

AU - Olesen, J.

PY - 2007

Y1 - 2007

N2 - Both calcitonin gene-related peptide (CGRP) and nitric oxide (NO) are potent vasodilators that have been shown to induce headache in migraine patients. Their antagonists are effective in the treatment of migraine attacks. In the present study, we hypothesize that vasodilation induced by the NO donor glyceryltrinitrate (GTN) or by CGRP is partially mediated via large conductance calcium-activated potassium (BK(Ca)) channels. The effects of the BK(Ca) channel selective inhibitor iberiotoxin on dural and pial vasodilation induced by CGRP, GTN and endogenously released CGRP by transcranial electrical stimulation (TES) were examined. Iberiotoxin significantly attenuated GTN-induced dural and pial artery dilation in vivo and in vitro, but had no effect on vasodilation induced by CGRP and TES. Our results show that GTN- but not CGRP-induced dural and pial vasodilation involves opening of BK(Ca) channels in rat.

AB - Both calcitonin gene-related peptide (CGRP) and nitric oxide (NO) are potent vasodilators that have been shown to induce headache in migraine patients. Their antagonists are effective in the treatment of migraine attacks. In the present study, we hypothesize that vasodilation induced by the NO donor glyceryltrinitrate (GTN) or by CGRP is partially mediated via large conductance calcium-activated potassium (BK(Ca)) channels. The effects of the BK(Ca) channel selective inhibitor iberiotoxin on dural and pial vasodilation induced by CGRP, GTN and endogenously released CGRP by transcranial electrical stimulation (TES) were examined. Iberiotoxin significantly attenuated GTN-induced dural and pial artery dilation in vivo and in vitro, but had no effect on vasodilation induced by CGRP and TES. Our results show that GTN- but not CGRP-induced dural and pial vasodilation involves opening of BK(Ca) channels in rat.

U2 - 10.1111/j.1468-2982.2007.01409.x

DO - 10.1111/j.1468-2982.2007.01409.x

M3 - Journal article

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SN - 0800-1952

VL - 27

SP - 1120

EP - 1127

JO - Cephalalgia, Supplement

JF - Cephalalgia, Supplement

IS - 10

ER -

Role of BKCa channels in cephalic vasodilation induced by CGRP, NO and transcranial electrical stimulation in the rat

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Role of BK_Ca channels in cephalic vasodilation induced by CGRP, NO and transcranial electrical stimulation in the rat