Existence of alpha(1A)- and alpha(1B)-adrenoceptor subtypes in canine mandibular alveolar arteries

1. The present study attempted to pharmacologically characterize the alpha-adrenoceptor subtypes mediating vasoconstriction in canine isolated and perfused mandibular alveolar artery (MAA). 2. Noradrenaline (NA) and phenylephrine (PE) induced a strong vasoconstriction in a dose-dependent manner. The PE-induced vascular constriction was significantly inhibited by treatment with prazosin. Xylazine evoked a moderate vascular constriction and the xylazine-induced response was suppressed by rauwolscine. The NA-induced response was partially inhibited by rauwolscine and the remaining response to NA was abolished by subsequent administration of prazosin. 3. Treatment of MAA with WB4101 produced a dose-dependent inhibition of NA-induced vasoconstriction. Pretreatment of tissues with 10 micromol/L chloroethylclonidine produced a slight and statistically significant inhibition of NA-induced responses. BMY 7378, a selective alpha(1D)-adrenoceptor antagonist, failed to significantly affect vasoconstrictor responses to NA. 4. The present results suggests that: (i) both alpha(1)- and alpha(2)-adrenoceptors are involved in vasoconstrictor responses in the canine MAA; and (ii) the alpha(1)-adrenoceptors involved in the vasoconstrictor responses in the MAA are characterized as mainly of the alpha(1A)- and partially of the alpha(1B)-adrenoceptor subtype.