ArticleBritish journal of pharmacology1996
Sources of calcium and alpha 1-adrenoceptor-mediated contraction in rat tail artery.
Article in British journal of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
1. The relative importance of intracellular and extracellular Ca2+ on alpha 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 microM and 10 microM) blocked by 50% (P < 0.001) and 75% (P < 0.001) respectively, the maximum contraction (Emax) induced by St-587. Nevertheless, to reach 40% inhibition of Emax on noradrenaline responses (P < 0.01), 10 microM 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. [3H]-prazosin binding to intact tail artery rings was saturable and of high affinity (KD = 4.44 +/- 0.46 nM; Bmax = 36.35 +/- 4.22 fmol mg-1 tissue). 6. Competition curves for inhibition of specific [3H]-prazosin binding by WB-4101 suggest that the rat tail artery contains two alpha 1-adrenoceptor subtypes in an approximate ratio of 60:40. 7. After irreversible alkylation of alpha 1B-adrenoceptors with 100 microM chloroethylclonidine (CEC), nifedipine (1 microM) 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 Ca2+ sources, on the alpha 1-adrenoceptor-mediated contraction, depends on the agonist used. The two alpha 1-adrenoceptor subtypes observed in binding experiments seem to be unrelated to the Ca2+ sources used for contraction.
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