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Keywords:

  • Human temporal artery;
  • α-CGRP-evoked relaxation;
  • BIBN4096BS;
  • CGRP(8-37);
  • migraine
  • Release of CGRP during migraine may produce harmful dilatation of cranial arteries, thereby possibly causing pain. We have compared the antagonism by BIBN4096BS and CGRP(8-37) of the relaxant effects of α-CGRP on rings of human temporal artery.

  • α-CGRP relaxed the arteries precontracted with 9 – 24 mM KCl (−logEC50=9.4) nearly as efficaciously as sodium nitroprusside (10 μM).

  • BIBN4096BS (0.1 – 100 nM) antagonized the effects of α-CGRP in surmountable manner with slopes of Schild-plots not different from unity. −LogKB values of 10.1 and 10.4 were estimated for BIBN4096BS when administered before or during the KCl-contracture respectively.

  • BIBN4096BS (1 μM) did not modify the relaxant effects of papaverine and sodium nitroprusside.

  • CGRP(8-37) (1 – 10 μM) antagonized the effects of α-CGRP in a surmountable manner with slopes of Schild-plots not different from unity. −LogKB values of 6.6 and 6.7 were estimated for CGRP(8-37) administered before or during the KCl-contracture respectively.

  • The high affinity of BIBN4096BS for CGRP receptors of human temporal artery makes it an excellent tool to explore the hypothesis of CGRP-evoked cerebral vasodilation in migraine.

British Journal of Pharmacology (2002) 136, 120–126; doi:10.1038/sj.bjp.0704682