The Effect of KATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers
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The Effect of KATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers. / Coskun, Hande; Elbahi, Fatima Azzahra; Al-Karagholi, Mohammad Al-Mahdi; Ghanizada, Hashmat; Sheykhzade, Majid; Ashina, Messoud.
In: Frontiers in Physiology, Vol. 12, 652136, 2021.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - The Effect of KATP 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
Y1 - 2021
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.
U2 - 10.3389/fphys.2021.652136
DO - 10.3389/fphys.2021.652136
M3 - Journal article
C2 - 34177610
VL - 12
JO - Frontiers in Physiology
JF - Frontiers in Physiology
SN - 1664-042X
M1 - 652136
ER -
ID: 272985687