Effects of sumatriptan on capsaicin-induced carotid haemodynamic changes and CGRP release in anaesthetized pigs
| Autor: | Pramod R. Saxena, Carlos M. Villalón, Jan P.C. Heiligers, Araceli Sánchez-López, Udayasankar Arulmani, Ingrid M. Garrelds, Edwin W Willems |
|---|---|
| Přispěvatelé: | Internal Medicine |
| Rok vydání: | 2004 |
| Předmět: |
Calcitonin Gene-Related Peptide
Migraine Disorders Sus scrofa Vasodilation Vagotomy Calcitonin gene-related peptide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Trigeminal Nerve 030212 general & internal medicine Trigeminal nerve Dose-Response Relationship Drug Sumatriptan business.industry Hemodynamics General Medicine medicine.disease Serotonin Receptor Agonists Carotid Arteries Nociception chemistry Migraine Capsaicin Anesthesia cardiovascular system Female Neurology (clinical) medicine.symptom business 030217 neurology & neurosurgery Vasoconstriction medicine.drug |
| Zdroj: | Cephalalgia, 24, 717-727. SAGE Publications Ltd |
| ISSN: | 1468-2982 0333-1024 |
| Popis: | 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 μg/kg, i.v.) on capsaicin-induced carotid haemodynamic changes and on CGRP release. Intracarotid (i.c.) infusions of capsaicin (10 μg/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 μg/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. |
| Databáze: | OpenAIRE |
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