SEARCH

SEARCH BY CITATION

Keywords:

  • α-adrenoceptor subtype;
  • BMY 7378;
  • cannula-inserting method;
  • chloroethylclonidine;
  • mandibular alveolar artery;
  • WB4101

SUMMARY

1. The present study attempted to pharmacologically characterize the α-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 μmol/L chloroethylclonidine produced a slight and statistically significant inhibition of NA-induced responses. BMY 7378, a selective α1D-adrenoceptor antagonist, failed to significantly affect vasoconstrictor responses to NA.

4. The present results suggests that: (i) both α1- and α2-adrenoceptors are involved in vasoconstrictor responses in the canine MAA; and (ii) the α1-adrenoceptors involved in the vasoconstrictor responses in the MAA are characterized as mainly of the α1A- and partially of the α1B-adrenoceptor subtype.