Increase in plasma calcitonin gene-related peptide from the extracerebral circulation during nitroglycerin-induced cluster headache attack

• Published in: Pain (Amsterdam) Vol. 60; no. 2; pp. 119 - 123
• Main Authors: Fanciullacci, Marcello, Alessandri, Massimo, Figini, Michela, Geppetti, Pierangelo, Michelacci, Sergio
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.02.1995; Elsevier
• Subjects: Adult; Biological and medical sciences; Calcitonin Gene-Related Peptide - blood; Calcitonin-gene related peptide; Cluster headache; Cluster Headache - blood; Cluster Headache - chemically induced; Cluster Headache - drug therapy; Humans; Male; Medical sciences; Neurology; Nitroglycerin; Remission Induction; Substance P; Substance P - blood; Sumatriptan; Sumatriptan - therapeutic use; Vascular diseases and vascular malformations of the nervous system; Cluster headache; Substance P; Sumatriptan; Nitroglycerin; Calcitonin-gene related peptide; Human; Pharmacologic test; Nervous system diseases; Nitroglycerine; Antimigrainous agent; Peptide hormone; Vasomotor headache; Cardiovascular disease; Exploration; Calcitonine gene related peptide; Neuropeptide; Cerebral disorder; Blood plasma; Vascular disease; Pain; Central nervous system disease; Cerebrovascular disease
• ISSN: 0304-3959; 1872-6623
• DOI: 10.1016/0304-3959(94)00097-X

In this study, changes in plasma levels of calcitonin gene-related peptide (CGRP) and substance P (SP) during a spontaneous-like cluster headache attack provoked by nitroglycerin were evaluated. Peptide variations after spontaneous or sumatriptan-induced remission were also assessed. Blood was collected from the external jugular vein homolateral to the pain side of 30 male cluster headache patients; 18 men were in an active and 12 in a remission one. Plasma levels of CGRP and SP were determined using sensitive radioimmunoassays for each peptide. CGRP-like immunoreactivity (CGRP-LI) was found to be augmented in patients in an active period and became elevated further at the peak of the provoked attack. A complete reversal occurred both after spontaneous and sumatriptan-induced remission. On the contrary, nitroglycerin neither provoked a cluster headache attack nor altered CGRP-LI in the patients in a remission period. The augmented levels of CGRP-LI measured before and after nitroglycerin administration, when the provoked attack reached the maximum intensity, suggest an activation of the trigeminovascular system during the active period of cluster headache. Moreover, the clinical and biochemical actions showed by sumatriptan stress the involvement of serotonin in cluster headache mechanisms.