Andersson Karl-Erik, Wein Alan J
Department of Clinical Pharmacology, Lund University Hospital, S-221 85 Lund, Sweden.
Pharmacol Rev. 2004 Dec;56(4):581-631. doi: 10.1124/pr.56.4.4.
The lower urinary tract constitutes a functional unit controlled by a complex interplay between the central and peripheral nervous systems and local regulatory factors. In the adult, micturition is controlled by a spinobulbospinal reflex, which is under suprapontine control. Several central nervous system transmitters can modulate voiding, as well as, potentially, drugs affecting voiding; for example, noradrenaline, GABA, or dopamine receptors and mechanisms may be therapeutically useful. Peripherally, lower urinary tract function is dependent on the concerted action of the smooth and striated muscles of the urinary bladder, urethra, and periurethral region. Various neurotransmitters, including acetylcholine, noradrenaline, adenosine triphosphate, nitric oxide, and neuropeptides, have been implicated in this neural regulation. Muscarinic receptors mediate normal bladder contraction as well as at least the main part of contraction in the overactive bladder. Disorders of micturition can roughly be classified as disturbances of storage or disturbances of emptying. Failure to store urine may lead to various forms of incontinence, the main forms of which are urge and stress incontinence. The etiology and pathophysiology of these disorders remain incompletely known, which is reflected in the fact that current drug treatment includes a relatively small number of more or less well-documented alternatives. Antimuscarinics are the main-stay of pharmacological treatment of the overactive bladder syndrome, which is characterized by urgency, frequency, and urge incontinence. Accepted drug treatments of stress incontinence are currently scarce, but new alternatives are emerging. New targets for control of micturition are being defined, but further research is needed to advance the pharmacological treatment of micturition disorders.
下尿路构成一个功能单元，受中枢和外周神经系统以及局部调节因子之间复杂的相互作用控制。在成年人中，排尿由脊髓-延髓-脊髓反射控制，该反射受脑桥以上结构的控制。几种中枢神经系统递质可以调节排尿，影响排尿的药物也可能如此；例如，去甲肾上腺素、γ-氨基丁酸或多巴胺受体及机制可能具有治疗作用。在周围，下尿路功能依赖于膀胱、尿道和尿道周围区域平滑肌和横纹肌的协同作用。包括乙酰胆碱、去甲肾上腺素、三磷酸腺苷、一氧化氮和神经肽在内的各种神经递质都参与了这种神经调节。毒蕈碱受体介导正常膀胱收缩以及膀胱过度活动症中至少主要部分的收缩。排尿障碍大致可分为储尿障碍或排空障碍。不能储存尿液可能导致各种形式的尿失禁，其中主要形式是急迫性尿失禁和压力性尿失禁。这些疾病的病因和病理生理学仍不完全清楚，这体现在目前的药物治疗包括相对较少的、或多或少有充分记录的选择这一事实上。抗毒蕈碱药物是膀胱过度活动症综合征药物治疗的主要手段，该综合征的特征是尿急、尿频和急迫性尿失禁。目前压力性尿失禁的公认药物治疗方法很少，但新的选择正在出现。控制排尿的新靶点正在被确定，但需要进一步研究以推进排尿障碍的药物治疗。
