1 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 eects of a-CGRP on rings of human temporal artery. 2 a-CGRP relaxed the arteries precontracted with 9 ± 24 mM KCl (7logEC 50 =9.4) nearly as ecaciously as sodium nitroprusside (10 mM). 3 BIBN4096BS (0.1 ± 100 nM) antagonized the eects of a-CGRP in surmountable manner with slopes of Schild-plots not dierent from unity. 7LogK B values of 10.1 and 10.4 were estimated for BIBN4096BS when administered before or during the KCl-contracture respectively. 4 BIBN4096BS (1 mM) did not modify the relaxant eects of papaverine and sodium nitroprusside. 5 CGRP(8-37) (1 ± 10 mM) antagonized the eects of a-CGRP in a surmountable manner with slopes of Schild-plots not dierent from unity. 7LogK B values of 6.6 and 6.7 were estimated for CGRP(8-37) administered before or during the KCl-contracture respectively. 6 The high anity 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.
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