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Vascular smooth muscle sensitivity to catecholamine-induced contraction is increased after catecholamine depletion by chemical sympathectomy and decreased after exogenous catecholα-mine administration. To investigate the role of the vascular o-adrenergic receptor in these alterations, we used the α-1 selective radioligand, (3H)-WB-4101, [phenoxy-3-H(JV)]-(2-(2,6-dimethoxyphenoxy- ethyl)aminomethyl-l,4-benzodioxane, to characterize the vascular postsynaptic a-adrenergic receptor in a membrane-rich particulate fraction of the rat mesenteric artery. Binding (3H)-WB-4101 was rapid, readily reversible, stereospecific, and saturable. Scatchard analysis described a single class of binding sites with a dissociation constant (Kd) of 0.76 ± 0.15 nM, and maximal binding capacity (B max ± 13 fmol/mg protein. Alpha-adrenergic agonists competed for the ()3H)-WB-4101 binding site in the α-edrenergic potency order of (-)-epinephrine (Kd = 3.0 /IM) > (-)-norepinephrine (Kd 8.8(-)-isoproterenol (Kd = 57 FIM), and the α-adrenergic antagonist phentolamine (Kd 7.6 nM) was 1000 times more potent than the /?-adrenergic antagonist, (±)-propranolol (Kd = 7400 nM). The number and affinity of α-adrenergic binding sites were studied in hyper- and hypo-adrenergic states. In mesenteric arteries from rats treated with exogenous epinephrine for 4 days, Bmal was decreased to 53 ± 10 fmol/ mg protein (n = 4, P < 0.01), whereas Kd for (3H)-WB-4101 was unchanged. Conversely, in mesenteric arteries from rats depleted of catecholamines with reserpine, Bmo, was unchanged (96 ± 15 fmol/mg protein), whereas Kd for (3H)-WB-4101 was decreased to 0.34 ± 0.07 nM (n = 6, P < 0.01), and Kd for (-)-epinephrine was decreased to 0.40 ± 0.19 μ (n = 6, P < 0.01). The effect of reserpine treatment was time dependent, being evident within 1 hour, and reaching a maximum after 3-7 days. The effects of catecholamine depletion with 6-hydroxydopamine were similar to those of reserpine. Thus, experimentally induced hyper- and hypo-adrenergic states can result in regulation of the vascular α-adrenergic receptor through changes in either receptor number or affinity. Circ Res 48: 104-111, 1981

Regulation of the postsynaptic alpha-adrenergic receptor in rat mesenteric artery. Effects of chemical sympathectomy and epinephrine treatment.