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逼尿肌肌细胞活动和传入信号。

Detrusor myocyte activity and afferent signaling.

机构信息

Wake Forest Institute for Regenerative Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA.

出版信息

Neurourol Urodyn. 2010;29(1):97-106. doi: 10.1002/nau.20784.

Abstract

AIMS

To discuss (1) mechanisms involved in the generation and control of myocyte contractions and consequent afferent nerve activity and (2) these mechanisms as targets for drugs aimed for treatment of overactive bladder (OAB) symptoms and detrusor overactivity (DO).

METHODS

Literature review of myocyte activation, bladder afferent nerves, mediators in the bladder, and translational aspects of the findings.

RESULTS

During bladder filling, there is normally no parasympathetic outflow from the spinal cord. Despite this, the bladder develops tone during filling and also exhibits non-synchronized local contractions and relaxations that are caused by a basal myogenic mechanical activity that may be reinforced by release of, for example, acetylcholine from non-neuronal and/or neuronal sources or local mediators, such as prostaglandins and endothelins. It is suggested that these spontaneous contractions are able to generate activity in afferent nerves ("afferent noise") that may contribute to DO and OAB.

CONCLUSIONS

Spontaneous bladder myocyte contractions and factors that are able to modulate them, as well as the consequent afferent nerve activity, may be targets for drugs meant for treatment of OAB/DO.

摘要

目的

讨论(1)肌细胞收缩的产生和控制机制以及随之而来的传入神经活动,以及(2)这些机制作为治疗膀胱过度活动症(OAB)症状和逼尿肌过度活动(DO)的药物靶点。

方法

对肌细胞激活、膀胱传入神经、膀胱介质以及这些发现的转化方面进行文献回顾。

结果

在膀胱充盈过程中,脊髓通常没有副交感神经传出。尽管如此,膀胱在充盈过程中仍会产生张力,并且还会表现出非同步的局部收缩和松弛,这是由基底肌源性机械活动引起的,这种活动可能会被例如乙酰胆碱从非神经元和/或神经元来源或局部介质(如前列腺素和内皮素)的释放所增强。有人认为,这些自发性收缩能够在传入神经中产生活动(“传入噪声”),这可能导致 DO 和 OAB。

结论

自发性膀胱肌细胞收缩及其能够调节这些收缩的因素,以及随之而来的传入神经活动,可能是治疗 OAB/DO 药物的靶点。

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