Urethral Sensations are Related to the Development of Detrusor Overactivity

作者:Yokoyama Osamu*; Miwa Yoshiji; Oyama Nobuyuki; Aoki Yoshitaka; Ito Hideaki; Tanase Kazuya; Ishida Hirokazu; Matsuta Yosuke; Kusukawa Naoya; Yamauchi Hiroki; Takahara Noriko; Watanabe Nozomu; Tsuchiyama Katsuki; Yokoi Satoshi; Akino Hironobu
来源:Lower Urinary Tract Symptoms, 2011, 3(2): 59-63.
DOI:10.1111/j.1757-5672.2011.00096.x

摘要

Urgency is the core symptom of the overactive bladder symptom complex, but the underlying mechanisms are not fully understood. Clinical findings have led to the assumption that bladder outlet obstruction (BOO) caused by benign prostatic enlargement (BPE) induces storage symptoms and detrusor overactivity. Presumably, BOO by BPE accounts for urgency; however, urgency is not always caused by BOO. Sensory nerves in the wall of the urethra fire in response to urethral fluid flow, and this activity initiates bladder contractions in the quiescent bladder and augments ongoing contractions in the active bladder. In humans, prostatic urethral anesthesia results in significant increases in bladder capacity among BPH patients without neurological diseases, therefore sensory stimuli from an anatomically altered prostatic urethra has the possibility to induce urgency and detrusor overactivity. Studies in animals demonstrate the basis for an excitatory urethra to bladder reflex. Urethral stimulation by prostaglandin E(2) induces an excitatory effect on micturition reflex by activation of C-fiber afferent nerves. alpha(1A)-adrenoceptor blocker has an inhibitory effect on the micturition reflex, suggesting excitatory urethra to bladder reflex is mediated by alpha(1A)-adrenoceptor. Even if there is no obstruction, increase in urethral sensory due to BPE may induce the development of the detrusor overactivity.

  • 出版日期2011-9