Bradykinin-induced vascular responses in dog isolated lingual artery.

1. Kinin-induced vascular responses were studied and kinin receptor subtypes were characterized in canine isolated and preconstricted lingual arteries. 2. A low dose of bradykinin (BK; < 3 x 10(-14) mol) induced only vasodilation, while a higher dose of BK (> 3 x 10(-13) mol) frequently induced a biphasic response: a transient constriction followed by dilation. 3. The BK-induced vasodilation was mostly endothelium dependent but was also partly endothelium independent because although the dilation response was greatly reduced after removal of the endothelium, it was not completely abolished. 4. The dilation response to BK was significantly inhibited by the B2 kinin receptor antagonist HOE 140 and was partly reduced by indomethacin (10 mumol/L) (P < 0.05). 5. Bradykinin-induced vasoconstriction was enhanced in endothelium-denuded preparations. The constriction was significantly inhibited by HOE 140 (10(-10) mol/L). The BK-induced responses were not affected by the B1 kinin receptor antagonist des-Arg9-[Leu8]-BK (3 x 10(-11) mol/L). 6. The B1 kinin receptor agonist des-Arg9-BK (> 10(-12) mol/L) produced vasodilation in 60% of endothelium-intact preparations. In 20% of the endothelium-intact preparations des-Arg9-BK produced a biphasic response: weak vasoconstriction followed by weak vasodilation. The des-Arg9-BK-induced dilation and constriction were significantly inhibited by des-Arg9-[Leu8]-BK (3 x 10(-11) mol/L), but were not affected by HOE 140 (10(-10) mol/L). 7. In conclusion, it appears that both B1 and B2 kinin receptors are present in the dog lingual artery. Both receptor subtypes mediate either vasodilation or vasoconstriction and BK-induced vasodilation is mostly endothelium dependent, although it may also be partially prostaglandin dependent.