Article date: August 1996
By: Antonia Tabernero, Nuria M. Vivas, Elisabet Vila, in Volume 118, Issue 8, pages 2067-2072
The relative importance of intracellular and extracellular Ca2+ on α1‐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.
Noradrenaline and St‐587 behaved as full agonists inducing a concentration‐dependent vasoconstriction.
Nifedipine (1 μm and 10 μm) 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 μm nifedipine was necessary.
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.
[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).
Competition curves for inhibition of specific [3H]‐prazosin binding by WB‐4101 suggest that the rat tail artery contains two α1‐adrenoceptor subtypes in an approximate ratio of 60:40.
After irreversible alkylation of α1B‐adrenoceptors with 100 μm chloroethylclonidine (CEC), nifedipine (1 μm) influenced to a greater extent the St‐587‐ than the noradrenaline‐induced contraction.
Our results indicate that the degree of participation of intracellular and extracellular Ca2+ sources, on the α1‐adrenoceptor‐mediated contraction, depends on the agonist used. The two α1‐adrenoceptor subtypes observed in binding experiments seem to be unrelated to the Ca2+ sources used for contraction.
The relative importance of intracellular and extracellular Ca2+ on α1‐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.
Noradrenaline and St‐587 behaved as full agonists inducing a concentration‐dependent vasoconstriction.
Nifedipine (1 μm and 10 μm) 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 μm nifedipine was necessary.
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.
[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).
Competition curves for inhibition of specific [3H]‐prazosin binding by WB‐4101 suggest that the rat tail artery contains two α1‐adrenoceptor subtypes in an approximate ratio of 60:40.
After irreversible alkylation of α1B‐adrenoceptors with 100 μm chloroethylclonidine (CEC), nifedipine (1 μm) influenced to a greater extent the St‐587‐ than the noradrenaline‐induced contraction.
Our results indicate that the degree of participation of intracellular and extracellular Ca2+ sources, on the α1‐adrenoceptor‐mediated contraction, depends on the agonist used. The two α1‐adrenoceptor subtypes observed in binding experiments seem to be unrelated to the Ca2+ sources used for contraction.
DOI: 10.1111/j.1476-5381.1996.tb15645.x
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