Phillippe M, Saunders T, Hariharan S
Department of Obstetrics and Gynecology, Michael Reese Hospital, Chicago, Illinois.
Life Sci. 1989;44(21):1555-62. doi: 10.1016/0024-3205(89)90449-9.
This study sought to evaluate alpha-2 and beta adrenergic modulation of cAMP production in the DDT1 MF-2 transformed smooth muscle myocyte. After stimulation with forskolin or adrenergic agonists with or without subtype specific antagonists, cAMP production was determined. These experiments confirmed an increase of cAMP in response to forskolin, isoproterenol, epinephrine, and norepinephrine; the adrenergic stimulation was inhibited by propranolol. On the other hand, the alpha-2 agonist clonidine did not inhibit cAMP production. Likewise, alpha-2 receptor blockade did not increase cAMP production in response to epinephrine. These studies, therefore, suggest that the DDT1 MF-2 myocyte does not contain a significant population of functional alpha-2 adrenergic receptors.
本研究旨在评估DDT1 MF-2转化的平滑肌心肌细胞中cAMP生成的α-2和β肾上腺素能调节。在用福斯高林或肾上腺素能激动剂刺激后,无论有无亚型特异性拮抗剂,均测定cAMP生成。这些实验证实,福斯高林、异丙肾上腺素、肾上腺素和去甲肾上腺素可使cAMP增加;肾上腺素能刺激被普萘洛尔抑制。另一方面,α-2激动剂可乐定不抑制cAMP生成。同样,α-2受体阻断也不会增加肾上腺素刺激引起的cAMP生成。因此,这些研究表明,DDT1 MF-2心肌细胞中不存在大量功能性α-2肾上腺素能受体。