Meng Jia, Ma Xue, Li Mingkai, Jia Min, Luo Xiaoxing
Department of Pharmacology, School of Pharmacy, The Fourth Military Medical University, Xian 710032, PR China.
Eur J Pharmacol. 2008 Jun 10;587(1-3):336-8. doi: 10.1016/j.ejphar.2008.03.019. Epub 2008 Mar 29.
The early research described that adrenocorticotropic hormone (ACTH) release from mouse pituitary tumor AtT-20 cells was regulated by histamine H(3) receptors. Here, we provide the evidence that histamine H(4) receptor was expressed in AtT-20 cell, and that the accelerated ACTH secretions from the cells by histamine and R-alpha-methylhistamine were blocked by JNJ7777120, a specific H(4) receptor antagonist, in concentration dependent manner, but not by the H(1) and H(2) receptor antagonists. The results indicate, for the first time, that histamine H(4) receptor, rather than histamine H(3) receptor, played a role in regulation of ACTH release from mouse pituitary AtT-20 cells.
早期研究表明,小鼠垂体瘤AtT-20细胞促肾上腺皮质激素(ACTH)的释放受组胺H(3)受体调节。在此,我们提供证据表明,组胺H(4)受体在AtT-20细胞中表达,并且组胺和R-α-甲基组胺诱导的该细胞ACTH分泌加速被特异性H(4)受体拮抗剂JNJ7777120以浓度依赖方式阻断,但不受H(1)和H(2)受体拮抗剂的影响。这些结果首次表明,在调节小鼠垂体AtT-20细胞ACTH释放中起作用的是组胺H(4)受体,而非组胺H(3)受体。