Skin microcirculatory effect of exogenous calcitonin gene-related peptide (CGRP) evaluated by laser Doppler flowmetry coupled with iontophoresis in healthy subjects

2007 ◽  
Vol 73 (2) ◽  
pp. 124-130 ◽  
Author(s):  
M. Rossi ◽  
A. Carpi ◽  
C. Di Maria ◽  
F. Galetta ◽  
G. Santoro
Keyword(s):  
Laser Doppler Flowmetry ◽  
Healthy Subjects ◽  
Calcitonin Gene Related Peptide ◽  
Laser Doppler ◽  
Doppler Flowmetry ◽  
Related Peptide ◽  
Calcitonin Gene

Increase in Meningeal Blood Flow by Nitric Oxide - Interaction with Calcitonin Gene-Related Peptide Receptor and Prostaglandin Synthesis Inhibition

Cephalalgia ◽  
2002 ◽  
Vol 22 (3) ◽  
pp. 233-241 ◽  
Author(s):  
T Strecker ◽  
M Dux ◽  
K Messlinger
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Cyclooxygenase Inhibitors ◽  
No Production ◽  
Doppler Flowmetry ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Meningeal Blood Flow

This study addresses possible interactions of the vasodilators nitric oxide (NO), calcitonin gene-related peptide (CGRP) and prostaglandins, which may be implicated in the generation of vascular headaches. Local application of the NO donator diethylamine-NONOate (NONOate) to the exposed dura mater encephali of the rat caused dose-dependent increases in meningeal blood flow recorded by laser Doppler flowmetry. Pre-application of the CGRP receptor antagonist CGRP8-37 significantly attenuated the evoked blood flow increases, while the cyclooxygenase inhibitors acetylsalicylic acid and metamizol were only marginally effective. Stimulation of rat dura mater with NONOate in vitro caused increases in CGRP release. NADPH- diaphorase activity indicating NO production was restricted to the endothelium of dural arterial vessels. We conclude that increases in meningeal blood flow caused by NO depend partly on the release and vasodilatory action of CGRP from dural afferents, while prostaglandins are not significantly involved.

scholarly journals CGRP release in an experimental human trigeminal pain model

Cephalalgia ◽  
2021 ◽  
pp. 033310242110172
Author(s):  
Achim Frese ◽  
Oliver Summ ◽  
Stefan Evers
Keyword(s):  
Healthy Subjects ◽  
Primary Headache ◽  
Calcitonin Gene Related Peptide ◽  
Headache Disorders ◽  
Pain Model ◽  
Related Peptide ◽  
Trigeminal Pain ◽  
Calcitonin Gene ◽  
Autonomic Activation ◽  
Mandibular Region

Background Migraine and trigemino-autonomic cephalalgia attacks are associated with an increase of α-calcitonin-gene related peptide levels in the ipsilateral jugular vein. It is however unknown whether trigeminal pain stimulation in healthy subjects without headache disorders also induces increase of calcitonin-gene related peptide levels. Findings We measured α-calcitonin-gene related peptide levels in eight healthy subjects after subcutaneous injection of capsaicin in the forehead and in the mandibular region and after injection of sodium chloride in the forehead. We observed a significant increase of α-calcitonin-gene related peptide level only after injection of capsaicin in the forehead (i.e. first trigeminal branch). We also observed trigemino-autonomic activation (lacrimation, rhinorrhea etc.) only after injection of capsaicin in the forehead. Conclusion Increase of α-calcitonin-gene related peptide levels do not only occur in primary headache attacks but also after experimental trigeminal pain of the first branch. This finding suggests that α-calcitonin-gene related peptide elevation is, at least an additional, unspecific effect of first trigeminal branch stimulation following pain activation and not a specific mechanism of idiopathic headache disorders.

scholarly journals The Influence of Calcitonin Gene-Related Peptide on Cerebral Hemodynamics in Nonmigraine Subjects with Calcitonin Gene-Related Peptide-Induced Headaches

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Matija Zupan ◽  
Marjan Zaletel ◽  
Darja Visočnik ◽  
Bojana Žvan
Keyword(s):  
Healthy Subjects ◽  
Calcitonin Gene Related Peptide ◽  
Carbon Dioxide Partial Pressure ◽  
Hemodynamic Changes ◽  
Time Points ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
End Tidal ◽  
Single Response ◽  
The Relationship

Background. Calcitonin gene-related peptide (CGRP) is regarded as an important molecule in trigeminovascular sensitization (TVS). CGRP-induced headaches (CGRP-IH) are evoked by intravascular administration of CGRP in nonmigraine and migraine subjects. CGRP might be associated with vasodilatation of the middle cerebral artery (MCA). It is unclear whether CGRP-induced hemodynamic changes relate to CGRP-IH in nonmigraine subjects. Methods. Twenty healthy subjects participated in our study. Polymodal recording of mean arterial velocity in MCA (vm MCA), end-tidal carbon dioxide partial pressure (Et-CO2), mean arterial pressure (MAP), and heart rate (HR) was employed using transcranial Doppler (TCD) sonography. During the experiment, we administered intravenous infusion of CGRP at a rate of 1.5 mcg/min. The vm MCA, Et-CO2, HR, and MAP were determined at time points T 0 , T 1 , T 2 , and T 3 . We calculated the responses at different time points and combined them into a single response vm MCAtot, Et-CO2tot, HRtot, and MAPtot. Results. We found significant differences along the time points in vm MCA ( p = < 0.001 ), Et-CO2 ( p = 0.003 ), MAP ( p < 0.001 ), and HR ( p < 0.001 ). The relationship between vm MCAtot and Et-CO2tot was significant and positive ( p = 0.005 ). The t -test showed significant differences between CGRP-IH and non-CGRP-IH subjects in vm MCAtot ( p = 0.021 ) but not in Et-CO2tot ( p = 0.838 ), MAPtot ( p = 0.839 ), and HRtot ( p = 0.198 ). Only vm MCAtot showed a significant relationship with CGRP-IH ( p = 0.028 ). Conclusions. Our study provides evidence for vasodilatation of MCA in relation to CGRP-IH due to intravascular CGRP detected by multimodal TCD. In the context of TVS induced by CGRP, MCA vasodilatation seems to represent an epiphenomenon of the underlying TVS.

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