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. 2003;5 Suppl 8(Suppl 8):S3-S10.

Neurophysiology of lower urinary tract function and dysfunction

Neurophysiology of lower urinary tract function and dysfunction

Naoki Yoshimura et al. Rev Urol. 2003.

Abstract

With the continued aging of the population, the incidence of conditions associated with bladder control will continue to grow. In this article, we review the neurophysiology and pathophysiology of the bladder and urethra and discuss logical concepts for the development of novel drug therapy that can better help the expanding population of patients with bladder control problems.

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Figures

Figure 1
Figure 1
Parasympathetic (pudendal nerve): Parasympathetic postganglionic nerve terminals release acetylcholine (ACh), which can excite various muscarinic receptors in bladder smooth muscles, leading to bladder contractions. ATP, adenosine triphosphate; NO, nitric oxide; cGMP, cyclic guanosine monophosphate.
Figure 2
Figure 2
Sympathetic (hypogastric nerve): Sympathetic postganglionic terminals that release norepinephrine (NE) elicit contractions of bladder base and urethral smooth muscle and relaxation of the bladder body.
Figure 3
Figure 3
Somatic (pudendal nerve): Somatic nerve terminals release acetylcholine (ACh), which acts on skeletal muscle-type nicotinic receptors (N) to induce a muscle contraction.
Figure 4
Figure 4
Normal control of micturition: The normal sensations of bladder filling appear to be mediated by small myelinated fibers.
Figure 5
Figure 5
Altered neurocontrol in overactive bladder and interstitial cystitis: C-fibers, which are normally “silent,” appear to have the specific function of signaling inflammatory or noxious events in the bladder.

References

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