Spontaneous Activity and the Urinary Bladder

Spontaneous Activity and the Urinary Bladder
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DOI:
10.1007/978-981-13-5895-1_5
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发表时间:
2019-01-01
期刊:
SMOOTH MUSCLE SPONTANEOUS ACTIVITY: PHYSIOLOGICAL AND PATHOLOGICAL MODULATION
影响因子:
--
通讯作者:
McCloskey, Karen D.
McCloskey, Karen D.
中科院分区:
其他
文献类型:
--
作者:
Fry, Christopher H.;McCloskey, Karen D.

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膀胱有两个功能:当它放松和高度顺应时储存尿液;当膀胱内压由于膀胱壁中逼尿肌平滑肌的协调收缩而升高时排出其内容物。叠加在该描述上的是两个观察结果:(1)正常的、松弛的膀胱发展为膀胱内压力的小的瞬时增加,其由局部膀胱壁运动反映;(2)病理性的、较大的压力变化(逼尿肌过度活动)可发生,其可引起不自主的尿丢失和/或逼尿肌过度活动。这些自发性收缩的特征对于理解:在充盈期间如何维持正常的膀胱顺应性以及逼尿肌过度活动的病理生理学是重要的。考虑自发性收缩如何起源应包括膀胱壁的结构复杂性。逼尿肌平滑肌层由粘膜覆盖,粘膜本身是泌尿系统的复杂结构,固有层包含感觉神经、微血管、间质细胞和弥漫性肌肉成分。这些包括逼尿肌的内在节律性;膀胱壁中非肌肉起搏细胞的调节;自主神经对逼尿肌的运动输入;邻近粘膜对逼尿肌兴奋性和收缩性的调节以及固有层成分的自发收缩。本章将考虑每个理论在正常和膀胱过度活动症的证据,以及它们的意义如何在衰老和发育过程中变化。对这些机制的进一步理解也可能发现新的药物靶点,以改善逼尿肌过度活动相关的大收缩的临床后果。
The urinary bladder has two functions: to store urine, when it is relaxed and highly compliant; and void its contents, when intravesical pressure rises due to co-ordinated contraction of detrusor smooth muscle in the bladder wall. Superimposed on this description are two observations: (1) the normal, relaxed bladder develops small transient increases of intravesical pressure, mirrored by local bladder wall movements; (2) pathological, larger pressure variations (detrusor overactivity) can occur that may cause involuntary urine loss and/or detrusor overactivity. Characterisation of these spontaneous contractions is important to understand: how normal bladder compliance is maintained during filling; and the pathophysiology of detrusor overactivity. Consideration of how spontaneous contractions originate should include the structural complexity of the bladder wall. Detrusor smooth muscle layer is overlain by a mucosa, itself a complex structure of urothelium and a lamina propria containing sensory nerves, micro-vasculature, interstitial cells and diffuse muscular elements.Several theories, not mutually exclusive, have been advanced for the origin of spontaneous contractions. These include intrinsic rhythmicity of detrusor muscle; modulation by non-muscular pacemaking cells in the bladder wall; motor input to detrusor by autonomic nerves; regulation of detrusor muscle excitability and contractility by the adjacent mucosa and spontaneous contraction of elements of the lamina propria. This chapter will consider evidence for each theory in both normal and overactive bladder and how their significance may vary during ageing and development. Further understanding of these mechanisms may also identify novel drug targets to ameliorate the clinical consequences of large contractions associated with detrusor overactivity.