• Capsaicin;
  • resiniferatoxin;
  • microcirculation;
  • vasodilatation;
  • trigeminal ganglion;
  • dura mater;
  • nasal mucosa;
  • hCGRP8–37;
  • vinpocetine
  • 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