抄録
The interaction between α- and β-adrenergic agonists was examined with respect to amylase release from rat parotid glands. The effect of hypothyroid status on this interaction was also compared with that in euthyroid rats. Both methoxamine and clonidine potentiated isoproterenol-induced amylase release from parotid glands of eu- and hypothyroid rats, but the α2-adrenoceptor-mediated response disappeared in the hypothyroid rats. Dibutyryl cyclic AMP, a second messenger of β-adrenergic agonists, also showed essentially the same results as those of isoproterenol, but potentiation of dibutyryl cyclic AMP-induced amylase release with α-adrenergic agonists was mediated through only α1-adrenoceptors in both groups. Calcium ion plays an important role in the interaction between α- and β-adrenergic agonists. These results suggest that the potentiating effect of α-adrenergic agonists may be mediated at least in part through an unknown mechanism at the step distal to cyclic AMP formation in both eu and hypothyroid rats.
