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α2C-Adrenoceptors mediate contractile responses to noradrenaline in the human saphenous vein

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We have investigated the subtype of α2-adrenoceptor mediating isometric contractions of human saphenous vein in comparison with α2-adrenoceptor ligand binding sites. Postjunctional α2-adrenoceptors in the human saphenous vein were investigated in terms of the ability of α2-adrenoceptor antagonists to shift the contractile potency of noradrenaline. The following antagonists were employed (potencies, pKB, in human saphenous vein in parentheses): chlorpromazine (6.98±0.24), BDF 8933 (7.60±0.06), prazosin (6.62±0.15), ARC 239 (7.19±0.15), yohimbine (7.23±0.09), HV 723 (7.52±0.14), WB 4101 (7.90±0.06), SKF 104078 (6.55±0.08), BRL 44408 (5.72±0.21). Antagonist potency at postjunctional α2-adrenoceptors was correlated with antagonist affinity at α2-adrenoceptor ligand binding sites in membranes of human platelet (α2A), rat kidney (α2B) and Sf9 cells expressing human recombinant receptors (α2C), labelled with [3H]yohimbine. The correlation with the postjunctional α2-adrenoceptor mediating contraction of the human saphenous vein was best for the human recombinant α2C-adrenoceptor ligand binding site (r=0.92, n=8, P<0.001), as compared to correlations with the α2B-adrenoceptor ligand binding site of rat kidney (r=0.62, n=8, n.s.) and with the α2A-adrenoceptor ligand binding site of human platelet (r=0.23, n=8, n.s.). It is concluded that the functional postjunctional α2-adrenoceptor mediating contractions of the human saphenous vein closely resembles the human recombinant α2C-adrenoceptor ligand binding site.

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Received: 23 September 1996 / Accepted: 3 December 1996

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Gavin, K., Colgan, MP., Moore, D. et al. α2C-Adrenoceptors mediate contractile responses to noradrenaline in the human saphenous vein. Naunyn-Schmiedeberg's Arch Pharmacol 355, 406–411 (1997). https://doi.org/10.1007/PL00004961

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  • DOI: https://doi.org/10.1007/PL00004961

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