Tyagi Pradeep
Associate Professor, William Beaumont School of Medicine, Royal Oak, MI.
Can Urol Assoc J. 2011 Oct;5(5 Suppl 2):S128-30. doi: 10.5489/cuaj.11181.
Conventional wisdom now agrees that symptoms of overactive bladder (OAB) seem to emanate from an aberration in the voiding reflex, leading to involuntary detrusor contractions of either neurogenic or myogenic origin. Furthermore, emerging evidence also encourages us to adopt a new paradigm, in which bladder urothelium is not just a simple barrier but an active contributor to bladder function. In this paradigm, aberration in sensory mechanisms emanating from the urothelium can also contribute to OAB symptoms through altered excitability of afferents in the bladder leading to increased bladder sensation. The high density of muscarinic receptors expressed on urothelium can not only mediate release of urothelium-derived inhibitory factor, but can also be seen as an alternative site of action for antimuscarinic drugs. Urothelium also expresses a host of other receptors such as TRPV1 and TRPM8, whose functional role is yet to be confirmed.
现在普遍认为，膀胱过度活动症（OAB）的症状似乎源于排尿反射异常，导致神经源性或肌源性的逼尿肌不自主收缩。此外，新出现的证据也促使我们采用一种新的模式，即膀胱尿路上皮不仅是一个简单的屏障，而且是膀胱功能的积极贡献者。在这种模式中，尿路上皮产生的感觉机制异常也可通过改变膀胱传入神经的兴奋性导致膀胱感觉增强，从而促成OAB症状。尿路上皮表达的高密度毒蕈碱受体不仅可介导尿路上皮源性抑制因子的释放，还可被视为抗毒蕈碱药物的另一个作用位点。尿路上皮还表达许多其他受体，如TRPV1和TRPM8，其功能作用尚未得到证实。
