Overactive bladder - Pharmacological aspects
Overactive bladder - Pharmacological aspects
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DOI：
10.1080/003655902320766006
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发表时间：
2002-01-01
影响因子：
--
通讯作者：
Andersson, KE
中科院分区：
文献类型：
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作者：
Andersson, KE
排尿反射可以由逼尿肌平滑肌细胞的收缩或扩张或由来自尿道的信号启动。研究表明，膀胱扩张引起膀胱尿道释放ATP，ATP可激活上皮下传入神经末梢上的P2 X（3）受体，引起神经放电。然而，最有可能的是，在膀胱充盈期间传入纤维的激活不仅涉及ATP，而且涉及抑制性和刺激性递质/介质的级联反应。这些机制可能是未来药物的靶点。在正常和功能紊乱的膀胱中，毒蕈碱受体刺激产生逼尿肌收缩的主要部分，但越来越多的证据表明，在疾病状态下，如神经源性膀胱、流出道梗阻、特发性逼尿肌不稳定、间质性膀胱炎，以及在老化的膀胱中，可能发生经由嘌呤能受体的非胆碱能激活。如果该激活成分不仅负责膀胱收缩的一部分，而且还负责膀胱过度活动症的症状，则应将其视为治疗干预的重要目标。药物阻断不同的P2 X受体亚型，或通过其他机制抵消膀胱收缩。例如β（3）-肾上腺素能受体刺激，可用于治疗膀胱过度活动症。
The micturition reflex can be initiated by contraction or distension of detrusor smooth muscle cells, or by signals from the urothelium. It has been shown that bladder distension causes release of ATP from the urothelium and that ATP can activate P2X(3) receptors on suburothelial afferent nerve terminals to evoke a neural discharge. However, most probably the activation of afferent fibres during bladder filling involves not only ATP, but a cascade of inhibitory and stimulatory transmitters/mediators. These mechanisms may be targets for future drugs. Both in the normal and functionally disturbed bladder, muscarinic receptor stimulation produces the main part of detrusor contraction, but evidence is accumulating that in disease states, such as neurogenic bladders, outflow obstruction, idiopathic detrusor instability, interstitial cystitis, and also in the ageing bladder, a non-cholinergic activation via purinergic receptors may occur. If this component of activation is responsible not only for part of the bladder contractions, but also for the symptoms of the overactive bladder, it should be considered an important target for therapeutic interventions. Drugs blocking different P2X receptor subtypes, or counteracting bladder contraction via other mechanisms. e.g. beta(3)-adrenoceptor stimulation, may be developed for treatment of the overactive bladder.