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The Effect of K ATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers

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@article{e155c1b7ffb249de9ec217444128fb92,
title = "The Effect of K ATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers",
abstract = "Background: Calcitonin gene-related peptide (CGRP) dilates cranial arteries and triggers headache. The CGRP signaling pathway is partly dependent on activation of ATP-sensitive potassium (K ATP ) channels. Here, we investigated the effect of the K ATP channel blocker glibenclamide on CGRP-induced headache and vascular changes in healthy volunteers.Methods: In a randomized, double-blind, placebo-controlled, cross-over study, 20 healthy volunteers aged 18-27 years were randomly allocated to receive an intravenous infusion of 1.5 μg/min CGRP after oral pretreatment with glibenclamide (glibenclamide-CGRP day) or placebo (placebo-CGRP day). The primary endpoints were the difference in incidence of headache and the difference in area under the curve (AUC) for headache intensity scores (0-14 h) between glibenclamide and placebo. The secondary endpoints were the difference in AUC for middle cerebral artery blood flow velocity (V MCA ), superficial temporal artery (STA) and radial artery (RA) diameter, facial flushing, heart rate (HR) and mean arterial blood pressure (MAP) (0-4 h) between glibenclamide and placebo.Results: We found no significant difference in the incidence of headache between glibenclamide-CGRP day (14/20, 70%) and placebo-CGRP day (19/20, 95%) (P = 0.06). The AUC for headache intensity, V MCA , STA, RA, facial skin blood flow, HR, and MAP did not differ between glibenclamide-CGRP day compared to placebo-CGRP day (P > 0.05).Conclusion: Pretreatment with a non-selective K ATP channel inhibitor glibenclamide did not attenuate CGRP-induced headache and hemodynamic changes in healthy volunteers. We suggest that CGRP-induced responses could be mediated via activation of specific isoforms of sulfonylurea receptor subunits of K ATP channel.",
keywords = "humans, migraine, glyburide, calcitonin-gene related peptide, cranial arteries",
author = "Hande Coskun and Elbahi, {Fatima Azzahra} and Al-Karagholi, {Mohammad Al-Mahdi} and Hashmat Ghanizada and Majid Sheykhzade and Messoud Ashina",
note = "Copyright {\textcopyright} 2021 Coskun, Elbahi, Al-Karagholi, Ghanizada, Sheykhzade and Ashina.",
year = "2021",
month = jun,
day = "11",
doi = "10.3389/fphys.2021.652136",
language = "English",
volume = "12",
pages = "1--10",
journal = "Frontiers in Physiology",
issn = "1664-042X",
publisher = "Frontiers Research Foundation",

}

RIS

TY - JOUR

T1 - The Effect of K ATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers

AU - Coskun, Hande

AU - Elbahi, Fatima Azzahra

AU - Al-Karagholi, Mohammad Al-Mahdi

AU - Ghanizada, Hashmat

AU - Sheykhzade, Majid

AU - Ashina, Messoud

N1 - Copyright © 2021 Coskun, Elbahi, Al-Karagholi, Ghanizada, Sheykhzade and Ashina.

PY - 2021/6/11

Y1 - 2021/6/11

N2 - Background: Calcitonin gene-related peptide (CGRP) dilates cranial arteries and triggers headache. The CGRP signaling pathway is partly dependent on activation of ATP-sensitive potassium (K ATP ) channels. Here, we investigated the effect of the K ATP channel blocker glibenclamide on CGRP-induced headache and vascular changes in healthy volunteers.Methods: In a randomized, double-blind, placebo-controlled, cross-over study, 20 healthy volunteers aged 18-27 years were randomly allocated to receive an intravenous infusion of 1.5 μg/min CGRP after oral pretreatment with glibenclamide (glibenclamide-CGRP day) or placebo (placebo-CGRP day). The primary endpoints were the difference in incidence of headache and the difference in area under the curve (AUC) for headache intensity scores (0-14 h) between glibenclamide and placebo. The secondary endpoints were the difference in AUC for middle cerebral artery blood flow velocity (V MCA ), superficial temporal artery (STA) and radial artery (RA) diameter, facial flushing, heart rate (HR) and mean arterial blood pressure (MAP) (0-4 h) between glibenclamide and placebo.Results: We found no significant difference in the incidence of headache between glibenclamide-CGRP day (14/20, 70%) and placebo-CGRP day (19/20, 95%) (P = 0.06). The AUC for headache intensity, V MCA , STA, RA, facial skin blood flow, HR, and MAP did not differ between glibenclamide-CGRP day compared to placebo-CGRP day (P > 0.05).Conclusion: Pretreatment with a non-selective K ATP channel inhibitor glibenclamide did not attenuate CGRP-induced headache and hemodynamic changes in healthy volunteers. We suggest that CGRP-induced responses could be mediated via activation of specific isoforms of sulfonylurea receptor subunits of K ATP channel.

AB - Background: Calcitonin gene-related peptide (CGRP) dilates cranial arteries and triggers headache. The CGRP signaling pathway is partly dependent on activation of ATP-sensitive potassium (K ATP ) channels. Here, we investigated the effect of the K ATP channel blocker glibenclamide on CGRP-induced headache and vascular changes in healthy volunteers.Methods: In a randomized, double-blind, placebo-controlled, cross-over study, 20 healthy volunteers aged 18-27 years were randomly allocated to receive an intravenous infusion of 1.5 μg/min CGRP after oral pretreatment with glibenclamide (glibenclamide-CGRP day) or placebo (placebo-CGRP day). The primary endpoints were the difference in incidence of headache and the difference in area under the curve (AUC) for headache intensity scores (0-14 h) between glibenclamide and placebo. The secondary endpoints were the difference in AUC for middle cerebral artery blood flow velocity (V MCA ), superficial temporal artery (STA) and radial artery (RA) diameter, facial flushing, heart rate (HR) and mean arterial blood pressure (MAP) (0-4 h) between glibenclamide and placebo.Results: We found no significant difference in the incidence of headache between glibenclamide-CGRP day (14/20, 70%) and placebo-CGRP day (19/20, 95%) (P = 0.06). The AUC for headache intensity, V MCA , STA, RA, facial skin blood flow, HR, and MAP did not differ between glibenclamide-CGRP day compared to placebo-CGRP day (P > 0.05).Conclusion: Pretreatment with a non-selective K ATP channel inhibitor glibenclamide did not attenuate CGRP-induced headache and hemodynamic changes in healthy volunteers. We suggest that CGRP-induced responses could be mediated via activation of specific isoforms of sulfonylurea receptor subunits of K ATP channel.

KW - humans

KW - migraine

KW - glyburide

KW - calcitonin-gene related peptide

KW - cranial arteries

UR - http://www.scopus.com/inward/record.url?scp=85121947030&partnerID=8YFLogxK

U2 - 10.3389/fphys.2021.652136

DO - 10.3389/fphys.2021.652136

M3 - Journal article

C2 - 34177610

VL - 12

SP - 1

EP - 10

JO - Frontiers in Physiology

JF - Frontiers in Physiology

SN - 1664-042X

M1 - 652136

ER -

ID: 66500595