Measurements of 45Ca2+ uptake and contractile responses after activation of postsynaptic alpha 1-adrenoceptors in the isolated canine saphenous vein: effects of calcium entry blockade.

The increase in 45Ca2+ content produced by the EC100 concentrations of a series of alpha 1-agonists in the canine saphenous vein (CSV) was determined in the presence of 10(-7) M rauwolscine and found to be correlated (r = 0.92) with the intrinsic activities of the alpha 1-agonists in CSV. The degree of inhibition of 45Ca2+ uptake by nifedipine (1 microM) was inversely correlated (r = -0.97) with the intrinsic activities of the alpha 1-agonists and also inversely correlated (r = -0.95) with the 45Ca2+ uptake induced by the agonists. In the presence of 5 mM LaCl3, there was no significant 45Ca2+ uptake elicited by KCl (80 mM) or activation of postsynaptic alpha 1-adrenoceptors in this tissue, and the alpha 1-agonists were found to have a varied ability to release internal Ca2+ for contractions. It is concluded that (1) activation of alpha 1-adrenoceptors in CSV utilizes both intracellular and extracellular Ca2+ for contractions; (2) the increase in 45Ca2+ content after activation of post-synaptic alpha 1-adrenoceptors in CSV is directly correlated with the intrinsic ability of the alpha 1-agonists to induce contractions; and (3) the sensitivity of the 45Ca2+ uptake to nifedipine is inversely related to the intrinsic ability of the alpha 1-agonists to translocate extracellular Ca2+.