Tamaoki J, Tagaya E, Isono K, Nagai A
First Department of Medicine, Tokyo Women's Medical College, Japan.
Biochem Biophys Res Commun. 1998 Jul 30;248(3):722-7. doi: 10.1006/bbrc.1998.9047.
We studied the existence of beta 3-adrenoceptors in canine pulmonary artery smooth muscle under isometric conditions in vitro. A rank order potency of vascular relaxation was isoproterenol > salbutamol > selective beta 3-adrenoceptor agonists, CL 316243 and BRL 37344. A marked desensitization to salbutamol occurred by pretreatment with salbutamol but not with CL 316243. When beta 1-adrenoceptors were blocked, the relaxant responses to salbutamol were competitively antagonized by the beta 2-adrenoceptor antagonist ICI 118551, whereas the response to CL 316243 was not. Cyanopindolol, a non-selective beta-adrenoceptor antagonist, antagonized CL 316243-induced relaxation in a competitive manner with a pA2 of 6.10, and this value was lower than that when salbutamol was used as an agonist (6.69). Intracellular cAMP levels were increased by CL 316243, an effect that was not altered by ICI 118551. Therefore, beta 3-adrenoceptors may be present and functioning in canine pulmonary artery.
我们在体外等长条件下研究了犬肺动脉平滑肌中β3-肾上腺素能受体的存在情况。血管舒张的效价顺序为异丙肾上腺素>沙丁胺醇>选择性β3-肾上腺素能受体激动剂CL 316243和BRL 37344。用沙丁胺醇预处理会导致对沙丁胺醇明显脱敏，但对CL 316243不会。当β1-肾上腺素能受体被阻断时，对沙丁胺醇的舒张反应被β2-肾上腺素能受体拮抗剂ICI 118551竞争性拮抗，而对CL 316243的反应则不会。非选择性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 316243诱导的舒张，pA2为6.10，该值低于以沙丁胺醇为激动剂时的值（6.69）。CL 316243可增加细胞内cAMP水平，ICI 118551不会改变这一效应。因此，β3-肾上腺素能受体可能存在于犬肺动脉中并发挥作用。
