Longhurst Penelope
Department of Basic and Pharmaceutical Sciences, Albany College of Pharmacy and Division of Urology, Albany Medical College, Albany, NY 12208-3492, USA.
Scand J Urol Nephrol Suppl. 2004(215):11-9. doi: 10.1080/03008880410015129.
A review was conducted of the current knowledge of fetal and postnatal development of autonomic bladder function in animals. Studies of fetal and neonatal bladder development have been done in many animal species. Development of normal bladder function requires coordination of a number of different systems and processes, and continues after birth during the early neonatal period. In many neonatal animals, micturition occurs only after stimulation of a perineal-to-bladder reflex triggered when the mother licks the perineal region, and bladder distension fails to stimulate micturition. Voiding resulting from the normal bladder-to-bladder spinobulbospinal reflex activated by bladder distension develops only slowly over the first few weeks of life as synaptic connections in the sacral parasympathetic nucleus mature. The neurogenic response of bladder strips from young neonates is more sensitive to inhibition by atropine than that of strips from older animals, suggesting that there are developmental changes in the contribution of non-adrenergic, non-cholinergic transmitters to the response of the bladder smooth muscle to intramural nerve stimulation. Release of acetylcholine from cholinergic nerves and the mechanisms required to transform muscarinic receptor stimulation into efficient bladder contraction and emptying are fully developed at birth, but contractile and relaxant responses to many other agonists, such as adenosine triphosphate and noradrenaline, are developmentally regulated. Changes in calcium influx and storage may be responsible for many of these changes. Fetal detrusor is exquisitely sensitive to nitric oxide. Electrical stimulation of precontracted fetal bladder strips causes relaxation, an effect that is not seen in adult tissues, and is decreased by inhibitors of the actions of nitric oxide. Development of bladder function occurs before the onset of puberty and therefore is not normally dependent on sex hormones. However, neonatal treatment with or depletion of sex hormones can modulate bladder function. In particular, alpha-adrenergic receptor-mediated contractile responses of bladder detrusor are increased by prepubertal castration, an effect that may result from increases in the density of alpha-adrenergic receptors and/or changes in alpha-adrenergic receptor subtype expression.
对动物自主膀胱功能的胎儿期和出生后发育的现有知识进行了综述。已在许多动物物种中开展了胎儿和新生儿膀胱发育的研究。正常膀胱功能的发育需要多个不同系统和过程的协调配合，并且在出生后的新生儿早期仍在继续。在许多新生动物中，排尿仅在母亲舔舐会阴区域触发会阴至膀胱反射刺激后才会发生，膀胱扩张无法刺激排尿。由膀胱扩张激活的正常膀胱至膀胱脊髓延髓脊髓反射引起的排尿在生命的最初几周内发展缓慢，因为骶副交感神经核中的突触连接逐渐成熟。与年长动物的膀胱条相比，年幼新生儿的膀胱条对阿托品抑制的神经源性反应更敏感，这表明非肾上腺素能、非胆碱能递质对膀胱平滑肌对壁内神经刺激反应的贡献存在发育变化。胆碱能神经释放乙酰胆碱以及将毒蕈碱受体刺激转化为有效的膀胱收缩和排空所需的机制在出生时已完全发育，但对许多其他激动剂（如三磷酸腺苷和去甲肾上腺素）的收缩和舒张反应受发育调节。钙内流和储存的变化可能是其中许多变化的原因。胎儿逼尿肌对一氧化氮极为敏感。对预先收缩的胎儿膀胱条进行电刺激会导致舒张，这一效应在成年组织中未见，并且一氧化氮作用抑制剂可减弱该效应。膀胱功能的发育在青春期开始之前就已发生，因此通常不依赖于性激素。然而，新生儿期给予性激素或消耗性激素可调节膀胱功能。特别是，青春期前阉割会增加膀胱逼尿肌α-肾上腺素能受体介导的收缩反应，这种效应可能是由于α-肾上腺素能受体密度增加和/或α-肾上腺素能受体亚型表达变化所致。
