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Titolo:
THE MODE OF ACTION OF SUMATRIPTAN IS VASCULAR - A DEBATE
Autore:
HUMPHREY PPA; GOADSBY PJ;
Indirizzi:
PRINCE HENRY HOSP,DEPT NEUROL SYDNEY NSW 2036 AUSTRALIA PRINCE HENRY HOSP,DEPT NEUROL SYDNEY NSW 2036 AUSTRALIA UNIV CAMBRIDGE,GLAXO INST APPL PHARMACOL CAMBRIDGE ENGLAND UNIV CAMBRIDGE,DEPT PHARMACOL CAMBRIDGE ENGLAND
Titolo Testata:
Cephalalgia
fascicolo: 6, volume: 14, anno: 1994,
pagine: 401 - 410
SICI:
0333-1024(1994)14:6<401:TMOAOS>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEUROGENIC PLASMA EXTRAVASATION; ANTIMIGRAINE DRUG SUMATRIPTAN; ISOLATED SAPHENOUS-VEIN; EXTRACEREBRAL CIRCULATION; TRIGEMINOVASCULAR SYSTEM; 5-HT1-LIKE RECEPTOR; CEREBRAL-ARTERIES; DURA-MATER; GUINEA-PIG; MIGRAINE;
Keywords:
MIGRAINE; NEURONAL; PATHOGENESIS; SUMATRIPTAN; VASCULAR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
P.P.A. Humphrey e P.J. Goadsby, "THE MODE OF ACTION OF SUMATRIPTAN IS VASCULAR - A DEBATE", Cephalalgia, 14(6), 1994, pp. 401-410

Abstract

Two mechanisms have been proposed to explain the primary mode of action of sumatriptan: vasoconstriction and trigeminal nerve terminal inhibition. Sumatriptan is a potent vasoconstrictor of intracranial arteries. It has been shown to increase blood flow velocity in large intracranial arteries in man in a dose-dependent fashion both during and between migraine attacks. Since the vasoconstrictor response of sumatriptan is reproducible outside the migraine attack, this action appears to be a direct vascular effect and not indirectly mediated via neural mechanisms. Sumatriptan also causes rapid constriction of dural and meningeal vessels in vivo. It does not modify cerebral blood now but does constrict arterio-venous anastamoses that may be dilated during a migraine attack. This evidence suggests that sumatriptan has a direct, dose-related vasoconstrictor action on certain intracranial blood vessels that correlates with its antimigraine activity. Alternatively, sumatriptan may act directly on the trigeminal sensory nerve terminals withinthe cranial blood vessel, inhibiting the release of sensory neuropeptides. Experimental data from animal studies have shown that following electrical stimulation of the trigeminal ganglion there is a neurogenic inflammatory response with plasma protein extravasation from dural blood vessels. This response can be significantly reduced by sumatriptan at a dose level similar to that used in clinical treatment. This finding is further supported by the clinical observation that sumatriptanreduces the plasma levels of calcitonin gene-related peptide which are raised during a migraine attack.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 09:32:11