Release of substance P, calcitonin gene-related peptide and prostaglandin E2 from rat dura mater encephali following electrical and chemical stimulation in vitro

Neuroscience ◽  
1999 ◽  
Vol 89 (3) ◽  
pp. 901-907 ◽  
Author(s):  
A Ebersberger ◽  
B Averbeck ◽  
K Messlinger ◽  
P.W Reeh
Keyword(s):  
Substance P ◽  
Prostaglandin E2 ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Chemical Stimulation ◽  
Dura Mater Encephali ◽  
Related Peptide ◽  
Calcitonin Gene

Release of Histamine from Dural Mast Cells by Substance P and Calcitonin Gene-Related Peptide

Cephalalgia ◽  
1997 ◽  
Vol 17 (3) ◽  
pp. 166-174 ◽  
Author(s):  
A Ottosson ◽  
L Edvinsson
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Histamine Release ◽  
Dura Mater ◽  
Neurogenic Inflammation ◽  
Calcitonin Gene Related Peptide ◽  
Sampling Procedure ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Peritoneal Mast Cells

The aim of the present study was to examine if the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) can stimulate histamine release from mast cells in the dura mater and thereby play a role in cranial vasoregulation and local neurogenic inflammation. Dura mater mast cells were compared with peritoneal mast cells in the rat. Histamine was released from dura mater mast cells by compound 48/80, SP and CGRP but from peritoneal mast cells only by compound 8/80 and SP. NPY and VIP released quite small amounts of histamine from dural mast cells. The release on SP and CGRP from rat dura mater mast cells was blocked by the receptor antagonists FK888 and CGRP8-37 respectively, suggesting receptor mediated release mechanisms. None of the stimuli released histamine from human or porcine dural mast cells, possibly because the sampling procedure injures and incapacitates the cells.

Cyclooxygenase Inhibitors Modify the Relaxant Effect of Vasoactive Intestinal Polypeptide and Substance P in Isolated Porcine Ophthalmic Artery

Cephalalgia ◽  
1992 ◽  
Vol 12 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Maurice B Vincent
Keyword(s):  
Substance P ◽  
Ophthalmic Artery ◽  
Calcitonin Gene Related Peptide ◽  
Cyclooxygenase Inhibitors ◽  
Plasma Extravasation ◽  
Relaxant Effect ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Ophthalmic Arteries

The absolute indomethacin effect in some unilateral headaches may, at least partially, be cyclooxygenase inhibition-independent. Aspirin and indomethacin, for example, may inhibit the neurogenically induced plasma extravasation in rat dura mater. Given the putative involvement of trigeminal neuropeptides in the pathophysiology of these conditions, the influence of cyclooxygenase inhibitors (indomethacin, acetylsalicylic acid (ASA) and naproxen) has been studied upon substance P, calcitonin gene-related peptide and vasoactive intestinal peptide (VIP)-induced vasodilatation in PGF2a precontracted porcine ophthalmic arteries in vitro. None of the cyclooxygenase inhibitors significantly altered the effects of calcitonin gene-related peptide. The 10-10 mol/1 VIP-induced relaxation was inhibited significantly by all three cyclooxygenase inhibitors. Substance P-induced relaxation (from 10-10 to 10-8 mol/l) was enhanced by ASA and inhibited both by naproxen and, to a lesser extent, by indomethacin. The results suggest mainly that VIP-induced relaxations, particularly at lower concentrations, may be inhibited by all three cyclooxygenase inhibitors, and that naproxen, to a greater extent than aspirin or indomethacin, showed a tendency to inhibit vasodilatation induced by all peptides.

Interaction of Calcitonin Gene-Related Peptide, Nitric Oxide and Histamine Release in Neurogenic Blood Flow and Afferent Activation in The Rat Cranial Dura Mater

Cephalalgia ◽  
2007 ◽  
Vol 27 (6) ◽  
pp. 481-491 ◽  
Author(s):  
N Schwenger ◽  
M Dux ◽  
R de Col ◽  
R Carr ◽  
K Messlinger
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Histamine Release ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Receptor Blockade ◽  
Cgrp Receptor ◽  
Related Peptide ◽  
Calcitonin Gene

Calcitonin gene-related peptide (CGRP), nitric oxide (NO) and histamine are implicated in primary headaches but their role in vascular and nociceptive events in the dura mater is not well described. In an in vitro preparation of the hemisected rat skull, CGRP and histamine release from the cranial dura was measured using enzyme-linked immunoassays. While the NO donator NONOate (10-4 M) was without effect, CGRP (10-5 M) induced considerable histamine release from the rat cranial dura, which was blocked by the CGRP receptor antagonist CGRP8-37 (10-5 M). Conversely, histamine (10-4 M) did not stimulate CGRP release. In vitro recordings from single rat meningeal afferents showed that only one of 12 mechanically identified units but several mechanically insensitive units responded to histamine (up to 10-5 M). Increases in meningeal blood flow after histamine application (10-4 M) to the rat cranial dura remained unchanged during CGRP receptor blockade with CGRP8-37, inhibition of NO synthesis with L-NAME (20 mg/kg i.v.) and H3 receptor blockade with thioperamide (10-4 M). We conclude that histamine produces direct vasodilatation and activates a subset of largely non-mechanically sensitive, non-CGRP containing afferents in the rat meninges. Histamine is released from meningeal mast cells which are stimulated by CGRP. Similar mechanisms may be involved in the pathogenesis of headaches.

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