大量科学文献支持的潜在的治疗应用NK-1拮抗剂治疗焦虑症。在一个生物性水平上,有一个解剖P物质之间的联系密切,NK-1受体和类。更具体地说,~ 50%的提升大脑5 -羟色胺神经元co-express P物质,和去甲肾上腺素细胞体在蓝斑表达NK-1受体。此外,它已经表明,NK-1受体封锁可以改变两个5 -羟色胺和去甲肾上腺素神经元的放电模式,增加海马神经发生。在功能层面上,NK-1拮抗剂(包括AV608)已经广泛展示活动几乎所有的传统临床化验确定抗焦虑剂,包括那些预测分析苯二氮卓类和选择性5 -羟色胺再摄取抑制剂(SSRIs)。临床上,焦虑仍然是一个高优先级的目标行业,就是明证这个地区最近的开发活动。众所周知,人类的肠道粘膜表达NK-1受体。这些受体平滑肌中还发现,小动脉、小静脉和细胞与淋巴结节和硝唑与P物质,这是发现在整个消化道。神经纤维,包括感觉纤维,进入与肥大细胞密切接触,也表达NK-1受体。此外,约有80%的内脏感觉传入纤维在肠道表达P物质,众所周知,NK-1受体在脊髓调解内脏痛觉过敏。 Tachykinins are potent secretagogues at the small and large intestinal mucosa in several animal models as well as in the human colon, where there is a direct NK-1 receptor mediated response. Perhaps most important with respect to IBS is the observation that stimulation of sensory fibers or mast cells in the human intestinal tract causes the release of substance P and a consequent increase in epithelial ion transport through the activation of NK-1 receptors. The response to colorectal distension has often been used as a proxy for IBS. In this model, colorectal distension increases abdominal flinching, which is an indicator of pain. This procedure also activates a rectocolonic inhibitory reflex characterized by a decrease in colonic pressure and an increase in fluid transport. Several authors have now observed that NK-1 receptors mediate this rectocolonic inhibitory reflex. Decreased colonic pressure is related to increased colonic transit and these findings are therefore consistent with reports that stress increases intestinal transit, an effect blocked by NK-1 receptor antagonists. Overactive bladder is a common and distressing condition that has a profound effect on the daily living of affected individuals. This common cause of urinary incontinence describes a cluster of symptoms typified by urinary urgency, frequency, and urge urinary incontinence. Whereas the currently available anticholinergic drugs used to treat overactive bladder act on efferent nerves to counteract overactive bladder, essentially after it occurs, NK-1 antagonists appear to have promising therapeutic potential in their ability to affect the afferent nerves that modulate bladder contraction. A key potential advantage of NK-1 antagonists is that there may be essentially no decrement of detrusor contractility and no urinary retention risk, as is seen with current anticholinergic agents. This is because NK-1 antagonists inhibit sensory afferent nerves but not efferent nerves, which are important for normal and complete voiding of urine. Furthermore, NK-1 antagonists have a more favorable tolerability profile than observed with anticholinergic medications.

目标	行动	生物
U神经激肽1受体	不可用	人类

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