CHARACTERIZATION OF GASTRIC ACID SECRATION BASED ON THE STUDY OF HISTAMINE H2 RECEPTOR AND HELICOBACTER PYROLI

histamine H2受体（H2 R）是主要抗ulcer药物的目标。H2拮抗剂在1970年代被广泛用于治疗性溃疡紊乱的方法，自1970年代以来，他们的发现。H2 R已被假定在胃半胱氨酸细胞中驻留，并将通过生成环腺苷单磷酸盐（cAMP）的方式进入胃酸的生产，但没有直接证据的半胱氨酸细胞已被介绍到日期。在本研究中，我们克隆了小鼠H2 R基因，并产生了一种特定的抗体，我们对H2 R免疫化学的垃圾和亚细胞本地化进行了研究。我们在中国仓鼠卵巢细胞（CHO）中表达了人类H2受体（HH 2 R），并直接调查了各种H2受体拮抗剂的影响。IT-066 inhibited D13-d1H tiotidine binding and histamine刺激cAMP production more potently than famotidine and ranitidine。在添加剂中，预先孵化IT-066标记的受污染物在广泛洗涤后会产生很长的影响。Paraformaldehyde fixation of cell blunted inhibition of cell blunted inhibition of ye-D13 ye-D1 H tiotidine binducing by preincubation with IT-066，但不是由famotidine或ranitidine preincubation by preincubation引起的。IT-066在HH 2 R上具有潜在和长期的拮抗剂。至少有一个IT-066绑定网站不是由famotidine、ranitidine或tiotidine共享的，并受paraformaldehyde影响。使用HH 2 R expressed CHO，我们也分析了N-阿尔法-甲基组氨酸（NMeH）对cAMP生产的影响。NMeH是一种H2受体的抑制剂，由H. pyroli在胃霉菌中生产。NMeH在cAMP生产条件下比在组胺方面更有潜力。Although NMeH通过H3受体抑制酸切，可能通过H2受体刺激性酸切。

The histamine H2 receptor (H2R) is a target for major anti-ulcer drugs. H2 antagonists have been widely used for the treatment of peptic ulcer disorders since their discovery in the 1970s. The H2R was assumed to reside in gastric parietal cells and to be involved in gastric acid production via production of cyclic adenosine monophosphate (cAMP), although no direct evidence of pariental cells have been presented to date. In this study, we cloned the mouse H2R gene and generated a specific antibody, we immunohistochemically investigated gastric and subcellular localization of H2R. Next, we expressed human H2 receptor (HH2R) in Chinese hamster ovary cells (CHO) and directly investigated the effects of various H2 receptor antagonists. IT-066 inhibited ィイD13ィエD1H tiotidine binding and histamine stimulated cAMP production more potently than famotidine and ranitidine. In addition, preincubation of IT-066 marked inhibtory effects long after extensive washing. Paraformaldehyde fixation of cells blunted inhibition of ィイD13ィエD1H tiotidine binding induced by preincubation with IT-066, but not that by preincubation with famotidine or ranitidine. IT-066 has potent and long-lasting antagonisms on HH2R. At least one of the IT-066 binding sites is not shared by famotidine, ranitidine, or tiotidine and it affected by paraformaldehyde. Using HH2R expressed CHO, we also analyzed the effect of N-alfa-methylhistamine (NMeH) on cAMP production. NMeH is an H2 receptor agonist and produced by H.pyroli in gastric mucosa. NMeH was more potent in terms of cAMP production than histamine. Although NMeH inhibit acid secration via H3 receptor, it may stimultanously stimulate acid secration via H2 receptor.