Antidromic Effect of Calcitonin Gene-Related Peptide Containing Nerves on Cerebral Arteries in Rats

Asari, Jun; Suzuki, Kyoichi; Matsumoto, Masato; Sasaki, Tatsuya; Kodama, Namio

doi:10.5387/fms.47.75

Cited by 2 publications

(1 citation statement)

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“…Several studies have shown that sensory nerves innervating the cerebral vasculature contain substance P and CGRP (6, 26). However, capsaicin-induced relaxation of guinea-pig isolated basilar artery is mediated by CGRP rather than by substance P (27, 28).…”

Section: Discussionmentioning

confidence: 99%

Effects of Sumatriptan on Capsaicin-Induced Carotid Haemodynamic Changes and CGRP Release in Anaesthetized Pigs

et al. 2004

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It is suggested that during a migraine attack capsaicin-sensitive trigeminal sensory nerves release calcitonin gene related peptide (CGRP), resulting in cranial vasodilatation and central nociception. Hence, inhibition of trigeminal CGRP release may prevent the above vasodilatation and, accordingly, abort migraine headache. Therefore, this study investigated the effects of sumatriptan (100 and 300 microg/kg, i.v.) on capsaicin-induced carotid haemodynamic changes and on CGRP release. Intracarotid (i.c.) infusions of capsaicin (10 microg/kg/min, i.c.) increased total carotid, arteriovenous anastomotic and capillary conductances as well as carotid pulsations, but decreased the difference between arterial and jugular venous oxygen saturations. Except for some attenuation of arteriovenous anastomotic changes, the capsaicin-induced responses were not affected by sumatriptan. Moreover, i.c. infusions of capsaicin (0.3, 1, 3 and 10 microg/kg/min, i.c.) dose-dependently increased the jugular venous plasma concentrations of CGRP, which also remained unaffected by sumatriptan. The above results support the contention that the therapeutic action of sumatriptan is mainly due to cranial vasoconstriction rather than trigeminal (CGRP release) inhibition.

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