Samama P, Pei G, Costa T, Cotecchia S, Lefkowitz R J
Department of Medicine (Cardiology), Duke University Medical Center, Durham, North Carolina 27710.
Mol Pharmacol. 1994 Mar;45(3):390-4.
The beta 2-adrenergic receptor undergoes isomerization between an inactive conformation (R) and an active conformation (R*). The formation of the active conformation of the receptor molecule can be promoted by adrenergic agonists or by mutations in the third cytoplasmic domain that constitutively activate the receptor. Here we show that, of several beta-adrenergic receptor-blocking drugs tested, only two, ICI 118551 and betaxolol, inhibit the basal signaling activity of the beta 2-adrenergic receptor, thus acting as negative antagonists. We document the molecular properties of the more efficacious ICI 118551; (i) it shows higher affinity for the inactive form of the receptor and (ii) it inhibits the spontaneous formation of a beta-adrenergic receptor kinase substrate by the receptor. These properties are opposite those of adrenergic agonists, indicating that, in a fashion reciprocal to that of agonists, negative antagonists promote the formation of an inactive conformation of the receptor.
β2 - 肾上腺素能受体在无活性构象(R)和活性构象(R*)之间发生异构化。受体分子活性构象的形成可由肾上腺素能激动剂或第三胞质结构域中的突变促进,这些突变可组成性激活受体。在此我们表明,在所测试的几种β - 肾上腺素能受体阻断药物中,只有ICI 118551和倍他洛尔两种药物抑制β2 - 肾上腺素能受体的基础信号传导活性,因此作为负性拮抗剂起作用。我们记录了更有效的ICI 118551的分子特性;(i)它对受体的无活性形式显示出更高的亲和力,并且(ii)它抑制受体自发形成β - 肾上腺素能受体激酶底物。这些特性与肾上腺素能激动剂的特性相反,表明负性拮抗剂以与激动剂相反的方式促进受体无活性构象的形成。