1. In this study we examined the involvement of 5-HT(1B) and 5-HT(1D) receptors in the vasocontractile response induced by 5-HT(1B/D)-receptor agonist sumatriptan in rabbit common carotid artery (CCA). 2. Immunoblotting experiments using specific antisera against 5-HT(1B) or 5-HT(1D) receptors revealed the presence of one weak (at 93 kD for 5-HT(1B) or at 105 kD for 5-HT(1D)) and one strong band (at 46 kD for 5-HT(1B) or at 52 kD for 5-HT(1D)) in CCA. 3. Sumatriptan-mediated vasocontractile response was antagonized by SB216641 with an apparent pKb value of 8.6, which was consistent with its affinity for 5-HT(1B) receptor. Antagonism by BRL15572 was weak and calculated apparent pKb (6.0) value was consistent with its affinity for 5-HT(1B) subtype (but not for 5-HT(1D) subtype). This result indicates insignificant or no involvement of 5-HT(1D) receptor in the vasocontractile response. 4. The vasocontractile response induced by sumatriptan was highly sensitive to pertussis toxin treatment of CCA. Nicardipine, a calcium channel blocker, also potently antagonized vasocontractile response induced by sumatriptan. 5. 5-HT, but not sumatriptan, stimulated inositol phosphate accumulation in CCA. 6. These results indicate that stimulation of 5-HT(1B) subtype activate a pertussis toxin (PTX) sensitive G protein (Go/Gi) and mediate vasocontraction, in which L-type voltage dependent calcium channels are involved.