Sources of calcium and α 1 ‐adrenoceptor‐mediated contraction in rat tail artery

1 The relative importance of intracellular and extracellular Ca 2+ on α 1 ‐adrenoceptor‐mediated contraction by noradrenaline and St‐587 has been studied and correlated with the binding characteristics in intact tail artery from Sprague‐Dawley rats. 2 Noradrenaline and St‐587 behaved as full agonists inducing a concentration‐dependent vasoconstriction. 3 Nifedipine (1 μ m and 10 μ m ) blocked by 50% ( P < 0.001) and 75% ( P < 0.001) respectively, the maximum contraction (E max ) induced by St‐587. Nevertheless, to reach 40% inhibition of E max on noradrenaline responses ( P < 0.01), 10 μ m nifedipine was necessary. 4 Both agonists induced a concentration‐dependent accumulation of inositol phosphates. Noradrenaline behaved as a full agonist and St‐587 as a partial agonist for this response. 5 [ 3 H]‐prazosin binding to intact tail artery rings was saturable and of high affinity ( K D = 4.44 ± 0.46 nM; B max = 36.35 ± 4.22 fmol mg −1 tissue). 6 Competition curves for inhibition of specific [ 3 H]‐prazosin binding by WB‐4101 suggest that the rat tail artery contains two α 1 ‐adrenoceptor subtypes in an approximate ratio of 60:40. 7 After irreversible alkylation of α 1B ‐adrenoceptors with 100 μ m chloroethylclonidine (CEC), nifedipine (1 μ m ) influenced to a greater extent the St‐587‐ than the noradrenaline‐induced contraction. 8 Our results indicate that the degree of participation of intracellular and extracellular Ca 2+ sources, on the α 1 ‐adrenoceptor‐mediated contraction, depends on the agonist used. The two α 1 ‐adrenoceptor subtypes observed in binding experiments seem to be unrelated to the Ca 2+ sources used for contraction.