Login I S, Trugman J M
Department of Neurology, University of Virginia School of Medicine, Charlottesville 22908.
Neuropharmacology. 1989 Jun;28(6):647-50. doi: 10.1016/0028-3908(89)90145-7.
In cultured rat anterior pituitary cells incubated for 30-180 min, PHNO caused a concentration-dependent inhibition of prolactin release (IC50 approximately 0.5 nM) with maximal suppression at 5 nM. Forskolin increased cyclic adenosine 3',5'-monophosphate (cAMP) generation by stimulating adenylate cyclase and PHNO inhibited this effect with the same concentration profile as for inhibition of prolactin release. Inhibitory effects of 0.5 nM PHNO on prolactin release and cAMP generation were abolished by coincubation with 10 nM haloperidol, a D2 dopamine receptor antagonist. Within 30 min, 0.5 nM PHNO blunted the stimulation of prolactin release due to 10 nM thyrotropin-releasing hormone (TRH) or angiotensin II (AII). Thus, PHNO appears to activate the D2 dopamine receptor to inhibit the formation of cAMP and the secretion of prolactin.
在培养的大鼠垂体前叶细胞中孵育30 - 180分钟后，PHNO引起催乳素释放的浓度依赖性抑制（IC50约为0.5 nM），在5 nM时抑制作用最大。福斯高林通过刺激腺苷酸环化酶增加环磷腺苷（cAMP）的生成，而PHNO以与抑制催乳素释放相同的浓度曲线抑制这种作用。与10 nM氟哌啶醇（一种D2多巴胺受体拮抗剂）共同孵育可消除0.5 nM PHNO对催乳素释放和cAMP生成的抑制作用。在30分钟内，0.5 nM PHNO减弱了由10 nM促甲状腺激素释放激素（TRH）或血管紧张素II（AII）引起的催乳素释放刺激。因此，PHNO似乎激活D2多巴胺受体以抑制cAMP的形成和催乳素的分泌。
