Article date: May 1999
By: Barna Peitl, Gábor Pethô, Róbert Pórszász, József Németh, János Szolcsányi, in Volume 127, Issue 2, pages 457-467
Antidromic vasodilatation and plasma extravasation to stimulation of the trigeminal ganglion or its perivascular meningeal fibres was investigated by laser‐Doppler flowmetry and 125I‐labelled bovin serum albumin in the dura mater and in exteroceptive areas (nasal mucosa, upper eyelid) of anaesthetized rats pretreated with guanethidine and pipecuronium.
Trigeminal stimulation at 5 Hz for 20 s elicited unilateral phasic vasodilatation in the dura and lasting response in the nasal mucosa. Resiniferatoxin (1–3 μg kg−1 i.v.), topical (1%) or systemic capsaicin pretreatment (300 mg kg−1 s.c. plus 1 mg kg−1 i.v.) did not inhibit the meningeal responses but abolished or strongly inhibited the nasal responses. Administration of vinpocetine (3 mg kg−1 i.v.) increased both basal blood flow and the dural vasodilatation to perivascular nerve stimulation.
Dural vasodilatation to trigeminal stimulation was not inhibited by the calcitonin gene‐related peptide‐1 receptor (CGRP‐1) antagonist hCGRP8–37 (15 or 50 μg kg−1 i.v). or the neurokinin‐1 receptor antagonist RP 67580 (0.1 mg kg−1 i.v.) although both antagonists inhibited the nasal response. Neither mucosal nor meningeal responses were inhibited by atropine (5 mg kg−1 i.v.), hexamethonium (10 mg kg−1 i.v.) or the vasoactive intestinal polypeptide (VIP) antagonist (p‐chloro‐D‐Phe6‐Leu17)VIP (20 μg kg−1 i.v.).
Plasma extravasation in the dura and upper eyelid elicited by electrical stimulation of the trigeminal ganglion was almost completely abolished in rats pretreated with resiniferatoxin (3 μg kg−1 i.v.).
It is concluded that in the rat meningeal vasodilatation evoked by stimulation of trigeminal fibres is mediated by capsaicin‐insensitive primary afferents, while plasma extravasation in the dura and upper eyelid and the vasodilatation in the nasal mucosa are mediated by capsaicin‐sensitive trigeminal fibres.
Antidromic vasodilatation and plasma extravasation to stimulation of the trigeminal ganglion or its perivascular meningeal fibres was investigated by laser‐Doppler flowmetry and 125I‐labelled bovin serum albumin in the dura mater and in exteroceptive areas (nasal mucosa, upper eyelid) of anaesthetized rats pretreated with guanethidine and pipecuronium.
Trigeminal stimulation at 5 Hz for 20 s elicited unilateral phasic vasodilatation in the dura and lasting response in the nasal mucosa. Resiniferatoxin (1–3 μg kg−1 i.v.), topical (1%) or systemic capsaicin pretreatment (300 mg kg−1 s.c. plus 1 mg kg−1 i.v.) did not inhibit the meningeal responses but abolished or strongly inhibited the nasal responses. Administration of vinpocetine (3 mg kg−1 i.v.) increased both basal blood flow and the dural vasodilatation to perivascular nerve stimulation.
Dural vasodilatation to trigeminal stimulation was not inhibited by the calcitonin gene‐related peptide‐1 receptor (CGRP‐1) antagonist hCGRP8–37 (15 or 50 μg kg−1 i.v). or the neurokinin‐1 receptor antagonist RP 67580 (0.1 mg kg−1 i.v.) although both antagonists inhibited the nasal response. Neither mucosal nor meningeal responses were inhibited by atropine (5 mg kg−1 i.v.), hexamethonium (10 mg kg−1 i.v.) or the vasoactive intestinal polypeptide (VIP) antagonist (p‐chloro‐D‐Phe6‐Leu17)VIP (20 μg kg−1 i.v.).
Plasma extravasation in the dura and upper eyelid elicited by electrical stimulation of the trigeminal ganglion was almost completely abolished in rats pretreated with resiniferatoxin (3 μg kg−1 i.v.).
It is concluded that in the rat meningeal vasodilatation evoked by stimulation of trigeminal fibres is mediated by capsaicin‐insensitive primary afferents, while plasma extravasation in the dura and upper eyelid and the vasodilatation in the nasal mucosa are mediated by capsaicin‐sensitive trigeminal fibres.
British Journal of Pharmacology (1999) 127, 457–467; doi:10.1038/sj.bjp.0702561
DOI: 10.1038/sj.bjp.0702561
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