scholarly journals Meningeal blood flow is controlled by H2 S-NO crosstalk activating a HNO-TRPA1-CGRP signalling pathway

2015 ◽  
Vol 173 (3) ◽  
pp. 431-445 ◽  
Author(s):  
Mária Dux ◽  
Christine Will ◽  
Birgit Vogler ◽  
Milos R Filipovic ◽  
Karl Messlinger
Keyword(s):  
Blood Flow ◽  
Signalling Pathway ◽  
Meningeal Blood Flow

scholarly journals High‐dose phenylephrine increases meningeal blood flow through TRPV1 receptor activation and release of calcitonin gene‐related peptide

2019 ◽  
Vol 24 (2) ◽  
pp. 383-397 ◽  
Author(s):  
Mária Dux ◽  
Alexandru Babes ◽  
Jessica Manchen ◽  
Julika Sertel‐Nakajima ◽  
Birgit Vogler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Receptor Activation ◽  
Calcitonin Gene Related Peptide ◽  
High Dose ◽  
Trpv1 Receptor ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Meningeal Blood Flow ◽  
Flow Through

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 Sensitization of the trigeminovascular system following environmental irritant exposure

Cephalalgia ◽  
2015 ◽  
Vol 35 (13) ◽  
pp. 1192-1201 ◽  
Author(s):  
Phillip Edward Kunkler ◽  
LuJuan Zhang ◽  
Jessica Joan Pellman ◽  
Gerry Stephen Oxford ◽  
Joyce Harts Hurley
Keyword(s):  
Blood Flow ◽  
Inhalation Exposure ◽  
Chemical Exposure ◽  
Male Rats ◽  
Mrna Levels ◽  
Trigeminovascular System ◽  
Flow Measurements ◽  
Cell Counts ◽  
Meningeal Blood Flow ◽  
Blood Flow Measurements

Background Air pollution is linked to increased emergency room visits for headache, and migraine patients frequently cite chemicals or odors as headache triggers, but the association between air pollutants and headache is not well understood. We previously reported that nasal administration of environmental irritants acutely increases meningeal blood flow via a TRPA1-dependent mechanism involving the trigeminovascular system. Here, we examine whether chronic environmental irritant exposure sensitizes the trigeminovascular system. Methods Male rats were exposed to acrolein, a TRPA1 agonist, or room air by inhalation for four days prior to meningeal blood flow measurements. Some animals were injected daily with a TRPA1 antagonist, AP-18, or vehicle prior to inhalation exposure. Trigeminal ganglia were isolated following blood flow measurements for immunocytochemistry and/or qPCR determination of TRPV1, TRPA1 and CGRP levels. Results Acrolein inhalation exposure potentiated blood flow responses both to TRPA1 and TRPV1 agonists compared to room air. Acrolein exposure did not alter TRPV1 or TRPA1 mRNA levels or TRPV1 or CGRP immunoreactive cell counts in the trigeminal ganglion. Acrolein sensitization of trigeminovascular responses to a TRPA1 agonist was attenuated by pre-treatment with AP-18. Interpretation These results suggest trigeminovascular sensitization as a mechanism for enhanced headache susceptibility after chemical exposure.

scholarly journals Adenosine and Migraine

1998 ◽  
Vol 25 (1) ◽  
pp. 55-58 ◽  
Author(s):  
R. Guieu ◽  
C. Devaux ◽  
H. Henry ◽  
G. Bechis ◽  
J. Pouget ◽  
...  
Keyword(s):  
Blood Flow ◽  
Migraine Without Aura ◽  
Complementary Treatment ◽  
Calcium Dependent ◽  
Migraine Headaches ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Meningeal Blood Flow ◽  
Dose Dependent ◽  
A2 Receptors

ABSTRACT:Background:Adenosine is a powerful natural vasodilator that participates in the control of cerebral and meningeal blood flow. In this context, it could be involved in the pathophysiology of migraine, since it was previously reported that intravenous adenosine can precipitate crises in migraine patients.Methods:We have investigated circulating adenosine levels in 12 patients suffering from migraine without aura, during crises and in crisis-free periods, and have compared the levels noted to those of a population of 10 controls. To determine if there are interactions between adenosine and serotonin, we examined the effect of adenosine and antagonists on the uptake and the release of (14C) serotonin by platelets.Results and conclusions:We have reached a dual conclusion: 1) during migraine headaches there is an increase (mean 68%) in circulating adenosine levels and this increase may participate in cephalalgia; 2) activation of A2 receptors by adenosine causes a dose-dependent inhibition of calcium-dependent serotonin uptake by platelets. This inhibition of uptake could participate in the rapid elimination of serotonin in migraine sufferers. As a result of this, the use of adenosine antagonists could be an effective complementary treatment for migraine.

Calcitonin gene related peptide released from dural nerve fibers mediates increase of meningeal blood flow in the rat

1995 ◽  
Vol 73 (7) ◽  
pp. 1020-1024 ◽  
Author(s):  
K. Meßlinger ◽  
U. Hanesch ◽  
M. Kurosawa ◽  
M. Pawlak ◽  
R. F. Schmidt
Keyword(s):  
Blood Flow ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Nerve Fibers ◽  
Dura Mater Encephali ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Meningeal Blood Flow ◽  
Meningeal Artery ◽  
Stimulation Of

The parietal dura mater encephali of the rat was shown by immunohistochemistry to be densely innervated by calcitonin gene related peptide (CGRP) immunoreactive nerve fibers spreading around the medial meningeal artery and its branches. Electrical stimulation of the dural surface (10–20 V, 5–10 Hz, 10–30 min) caused a depletion of CGRP-immunopositive fibers, suggesting a release of CGRP. The dural blood flow around branches of the medial meningeal artery was also monitored with a laser Doppler flowmeter. Short periods (30 s) of electrical stimulation with parameters that presumably released CGRP from nerve fibers caused a repeatable and constant increase of the blood flow for 1–2 min. This evoked increase could dose dependently be inhibited by topical application of the CGRP antagonist hCGRP8–37. Accordingly, administration of hCGRP increased the basal blood flow. We conclude that stimulation of trigeminal afferents innervating the dura mater releases CGRP from peptidergic afferent terminals, thereby causing vasodilatation and increasing the meningeal blood flow, an important element of neurogenic inflammation.Key words: dura mater encephali, afferent nerve fibers, calcitonin gene related peptide, immunohistochemistry, laser Doppler flowmetry.

scholarly journals Involvement of TRPA1 receptors in meningeal blood flow induced by formation of nitroxyl (NO-/HNO)

2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
M Dux ◽  
M Eberhardt ◽  
MR Filipovic ◽  
R DeCol ◽  
K Messlinger
Keyword(s):  
Blood Flow ◽  
Meningeal Blood Flow

H 2 S-NO-TRPA1-CGRP signalling controls meningeal blood flow

Neuropeptides ◽  
2017 ◽  
Vol 65 ◽  
pp. 130
Author(s):  
Maria Dux ◽  
Christine Will ◽  
Birgit Vogler ◽  
Milos R. Filipovic ◽  
Karl Messlinger
Keyword(s):  
Blood Flow ◽  
Meningeal Blood Flow

scholarly journals Inhibition of stimulated meningeal blood flow by a calcitonin gene-related peptide binding mirror-image RNA oligonucleotide

2006 ◽  
Vol 148 (4) ◽  
pp. 536-543 ◽  
Author(s):  
Thomas Denekas ◽  
Markus Tröltzsch ◽  
Axel Vater ◽  
Sven Klussmann ◽  
Karl Messlinger
Keyword(s):  
Blood Flow ◽  
Peptide Binding ◽  
Calcitonin Gene Related Peptide ◽  
Mirror Image ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Meningeal Blood Flow

scholarly journals TRESK background potassium channel modifies the TRPV1-mediated nociceptor excitability in sensory neurons

Cephalalgia ◽  
2021 ◽  
pp. 033310242198926
Author(s):  
Miklós Lengyel ◽  
Dominika Hajdu ◽  
Alice Dobolyi ◽  
Judit Rosta ◽  
Gábor Czirják ◽  
...  
Keyword(s):  
Blood Flow ◽  
Dorsal Root Ganglion ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Calcitonin Gene ◽  
Meningeal Blood Flow ◽  
Ganglion Neurons ◽  
Knockout Animals

Background TWIK-related spinal cord potassium channel (TRESK) background potassium channels have a key role in controlling resting membrane potential and excitability of sensory neurons. A frameshift mutation leading to complete loss of TRESK function has been identified in members of a family suffering from migraine with aura. In the present study, we examined the role of TRESK channels on nociceptor function in mice. Methods Calcium imaging was used to investigate the role of TRESK channels in the modulation of the response evoked by transient receptor potential vanilloid 1 (TRPV1) receptor stimulation in dorsal root ganglion neurons. Release of calcitonin gene-related peptide from trigeminal afferents and changes in meningeal blood flow were also measured. Experiments were performed on wild-type and TRESK knockout animals. Results Inhibition of TRESK increased the TRPV1-mediated calcium signal in dorsal root ganglion neurons and potentiated capsaicin-induced increases in calcitonin gene-related peptide release and meningeal blood flow. Activation of TRESK decreased the capsaicin sensitivity of sensory neurons, leading to an attenuation of capsaicin-induced increase in meningeal blood flow. In TRESK knockout animals, TRPV1-mediated nociceptive reactions were unaffected by pretreatment with TRESK modulators. Conclusions Pharmacological manipulation of TRESK channels influences the TRPV1-mediated functions of nociceptors. Altered TRESK function might contribute to trigeminal nociceptor sensitization in migraine patients.

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