Tagaya E, Tamaoki J, Takemura H, Isono K, Nagai A
First Department of Medicine, Tokyo Womens Medical College.
Nihon Kokyuki Gakkai Zasshi. 1998 May;36(5):433-7.
To examine possible contributions of beta(3)-adrenoceptors to catecholamine-induced pulmonary vasodilation, we studied isolated canine pulmonary arterial segments under isometric conditions. Addition of beta-adrenoceptor agonists produced a concentration-dependent relaxation of tissues precontracted with 50 mM KCl; the rank order of potency was isoproterenol (ISO, 1) > salbutamol (SAL, 0.97) > selective beta(3)-adrenoceptor agonists CL 316243 (CL, 0.87) and BRL 37344 (BRL, 0.86). Relaxant responses to SAL were competitively antagonized by the beta(2)-adrenoceptor antagonist ICI 118551 and the pA2 value was 6.67 +/- 0.21 (mean +/- SE), whereas the response to CL was weekly antagonized only by a high concentration of ICI 118551 (10(-5) M) and the apparent pA2 value was 5.24 when alpha-and beta(1)-adrenergic receptors were blocked. By contrast, the atypical beta-adrenoceptor antagonist cyanopindolol antagonized CL-induced relaxation in a competitive manner; the pA2 value was 6.71 +/- 0.12, which was lower than that with salbutamol (p < 0.05). Intracellular cyclic AMP levels were increased in a contraction-dependent manner by CL. These results suggest that beta(3)-adrenoceptors may exist in canine pulmonary arterial smooth muscle and that stimulation of this atypical receptor causes vasodilation through a cyclic AMP-dependent pathway.
为了研究β(3)-肾上腺素能受体在儿茶酚胺诱导的肺血管舒张中的可能作用，我们在等长条件下研究了离体犬肺动脉段。添加β-肾上腺素能受体激动剂可使预先用50 mM氯化钾预收缩的组织产生浓度依赖性舒张；效价顺序为异丙肾上腺素（ISO，1）>沙丁胺醇（SAL，0.97）>选择性β(3)-肾上腺素能受体激动剂CL 316243（CL，0.87）和BRL 37344（BRL，0.86）。β(2)-肾上腺素能受体拮抗剂ICI 118551竞争性拮抗对SAL的舒张反应，pA2值为6.67±0.21（平均值±标准误），而对CL的反应仅在高浓度ICI 118551（10(-5) M）时受到微弱拮抗，当α和β(1)-肾上腺素能受体被阻断时，表观pA2值为5.24。相比之下，非典型β-肾上腺素能受体拮抗剂氰吲哚洛尔以竞争性方式拮抗CL诱导的舒张；pA2值为6.71±0.12，低于沙丁胺醇（p<0.05）。CL以收缩依赖性方式增加细胞内环磷酸腺苷水平。这些结果表明，β(3)-肾上腺素能受体可能存在于犬肺动脉平滑肌中，刺激这种非典型受体可通过环磷酸腺苷依赖性途径引起血管舒张。
