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Decreased sensitivity of 5-HT1D receptors in chronic tension-type headache.

AbstractOBJECTIVE:
To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe.
BACKGROUND:
Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo.
METHODS:
We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo.
RESULTS:
Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P<0.01 and <0.05) altered in CTTH patients in comparison with controls.
CONCLUSION:
Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.
AuthorsI Rainero, W Valfrè, L Savi, M Ferrero, P Del Rizzo, P Limone, G C Isaia, L Gianotti, A Pollo, R Verde, F Benedetti, L Pinessi
JournalHeadache (Headache) Vol. 42 Issue 8 Pg. 709-14 (Sep 2002) ISSN: 0017-8748 [Print] United States
PMID12390633 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Receptor, Serotonin, 5-HT1D
  • Receptors, Serotonin
  • Serotonin Receptor Agonists
  • Sumatriptan
  • Prolactin
  • Growth Hormone
Topics
  • Adult
  • Brain (metabolism)
  • Chronic Disease
  • Female
  • Growth Hormone (blood, drug effects, metabolism)
  • Humans
  • Male
  • Prolactin (drug effects, metabolism)
  • Receptor, Serotonin, 5-HT1D
  • Receptors, Serotonin (drug effects, metabolism)
  • Serotonin Receptor Agonists (metabolism, pharmacology)
  • Sumatriptan (metabolism, pharmacology)
  • Tension-Type Headache (metabolism)

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