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Am J Physiol Renal Physiol 284: F840-F851, 2003; doi:10.1152/ajprenal.00187.2002
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Vol. 284, Issue 4, F840-F851, April 2003

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

Chiang-Ting Chien1,*, Hong-Jeng Yu2,*, Tser-Bin Lin5, Ming-Kuen Lai3, and Su-Ming Hsu4

Departments of 1 Medical Research, 2 Urology, 3 Medicine, and 4 Pathology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei 10022; and 5 Department of Physiology, Chung Shan Medical and Dental College, Taichung, Taiwan

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.

reactive oxygen species; micturition reflex; neurokinin receptor

* C.-T. Chien and H.-J. Yu contributed equally to this work.




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