Role of extracellular calcium in contractions produced by activation of postsynaptic alpha-2 adrenoceptors in the canine saphenous vein.

Canine saphenous vein (CSV) has been shown to contain both postsynaptic alpha-1 and alpha-2 adrenoceptors. Our previous studies have shown that activation of postsynaptic alpha-1 adrenoceptors in this tissue utilizes both extracellular and intracellular Ca++ to produce contractions. In the present study, the source of calcium mobilized by activation of postsynaptic alpha-2 adrenoceptors in CSV was elucidated. Contractions of tissue rings to the supramaximal concentrations of three selective alpha-2 agonists, B-HT 920, M-7 and clonidine, were determined in the absence and presence of 5 mM La . In the presence of La , clonidine and M-7 produced small but statistically significant contractions (8-14% of control) which were abolished when the alpha-1 adrenoceptors were inactivated by phenoxybenzamine (10(-7) M, 30 min). In contrast, contractions to B-HT 920 were abolished completely in the presence of La . All the three alpha-2 agonists stimulated 45Ca++ uptake into CSV (0.3-0.4 mmol/kg wet weight, 10 min). 45Ca++ efflux studies demonstrated that the selective alpha-2 agonist, B-HT 920 (10(-5) M plus 10(-7) M phenoxybenzamine), did not induce an increase in the rate of 45Ca++ efflux. In contrast, an augmented 45Ca++ efflux rate was observed with the alpha-1 agonist, phenylephrine (10(-4) M plus 10(-7) M rauwolscine). These results suggest that activation of postsynaptic alpha-2 adrenoceptors in CSV utilizes primarily extracellular Ca++ to produce contractions.