Substance P via NK1 receptor facilitates hyperactive bladder afferent signaling via action of ROS

Chiang Ting Chien*, Hong Jeng Yu, Tser Bin Lin, Ming Kuen Lai, Su Ming Hsu


研究成果: 雜誌貢獻期刊論文同行評審

90 引文 斯高帕斯(Scopus)


We explored whether substance P (SP) via neurokinin (NK) receptor facilitates bladder afferent signaling and reactive oxygen species (ROS) formation in bladder in association with neurogenic inflammation. We evaluated ROS activity and cystometrograms as well as pelvic nervous activity in anesthetized rat bladder with SP stimulation. Our results showed that endogenous SP via NK1, not NK2, receptor mediated a micturition reflex. An increase in SP by electrical stimulation of the pelvic nerve or an increase in exogenous SP by intra-arterial or intrathecal administration can facilitate myogenic and neurogenic bladder contractions. Furthermore, exaggerated SP release increased ROS in the bladder and whole blood via increased mast cell degranulation, intercellular adhesion molecule expression, and leukocyte adhesion, a primary source of ROS in the inflamed bladder. Treatment with NK1-receptor antagonists or ROS scavengers reduced bladder intercellular adhesion molecule expression and ROS and ameliorated the hyperactive bladder response. Our study indicates that the mechanism by which SP participates in the neurogenic bladder may be complicated by its proinflammatory activity and its ability to stimulate ROS generation.

頁(從 - 到)F840-F851
期刊American Journal of Physiology - Renal Physiology
發行號4 53-4
出版狀態已發佈 - 2003 4月 1

ASJC Scopus subject areas

  • 生理學
  • 泌尿科學


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