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.

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 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 Mechanisms of calcitonin gene-related peptide-induced increases of pulmonary blood flow in fetal sheep

2000 ◽  
Vol 279 (4) ◽  
pp. H1654-H1660 ◽  
Author(s):  
Yasushi Takahashi ◽  
Maartje De Vroomen ◽  
Christine Roman ◽  
Michael A. Heymann
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arteries ◽  
Calcitonin Gene Related Peptide ◽  
Fetal Sheep ◽  
Nitric Oxide Synthase Inhibitor ◽  
Flow Transducer ◽  
Related Peptide ◽  
Calcitonin Gene

Fetal pulmonary blood flow is regulated by various vasoactive substances. One, calcitonin gene-related peptide (CGRP), increases pulmonary blood flow. We examined four key physiological mechanisms underlying this response using the blocker drugs CGRP receptor blocker (CGRP8–37), nitric oxide synthase inhibitor [ N ω-nitro-l-arginine (l-NNA)], adenosine triphosphate-dependent potassium (KATP) channel blocker (glibenclamide), and cyclooxygenase inhibitor (indomethacin) in 17 near-term fetal sheep. Catheters were placed in the left (LPA) and main pulmonary arteries, and an ultrasonic flow transducer was placed around the LPA to measure flow continuously. CGRP was injected directly into the LPA (mean 1.02 μg/kg) before and after blockade, and responses to CGRP were statistically compared. Before blockade, CGRP increased LPA blood flow from 23 ± 25 to 145 ± 77 ml/min (means ± SD), and these increases were significantly attenuated by CGRP8–37( n = 6; 91% inhibition), l-NNA ( n = 6; 86% inhibition), and glibenclamide ( n = 6; 69% inhibition). No significant changes were found with indomethacin ( n = 6; 4% inhibition). Thus, in the fetal pulmonary circulation, CGRP increases pulmonary blood flow not only through its specific receptor but also, in part, through nitric oxide release and KATP channel activation.

Regional hemodynamic effects of calcitonin gene-related peptide

1989 ◽  
Vol 256 (2) ◽  
pp. R332-R338 ◽  
Author(s):  
S. M. Gardiner ◽  
A. M. Compton ◽  
T. Bennett
Keyword(s):  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Calcitonin Gene Related Peptide ◽  
Renal Vascular Resistance ◽  
High Dose ◽  
Base Line ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
The Common ◽  
Renal Vascular

Cardiovascular responses to infusions of rat alpha-calcitonin gene-related peptide (CGRP; 0.06, 0.6, 6.0 nmol/h) or rat alpha-atrial natriuretic peptide (ANP; 3.7 nmol/h) were measured in conscious rats. During infusion of the low dose of CGRP, when mean arterial pressure (MAP) was little affected, there were reductions in common carotid, renal, mesenteric, and hindquarter vascular resistances (the magnitude of the responses in the same descending order). However, only flow in the common carotid vessels was increased above base line. After infusion, there was a hindquarter vasoconstriction. During infusion of the higher doses of CGRP, there were dose-related decreases in MAP and increases in heart rate associated with (hyperemic) hindquarter vasodilatations and mesenteric vasoconstrictions. The common carotid vasodilatation peaked with the intermediate dose of CGRP; the changes in renal vascular resistance were not dose related. After infusion of the high dose of CGRP there were persistent (at least 60 min) common carotid and hindquarter vasodilatations and mesenteric vasoconstriction, with a transient overshoot in renal vascular resistance. Infusions of CGRP and ANP matched for their effects on MAP had similar influences on mesenteric hemodynamics, but all other variables were affected differently.

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