Adrenergic and capsaicin evoked nitric oxide release from urothelium and afferent nerves in urinary bladder. Birder, Lori A., Gerard Apodaca, William C. De Groat, and Anthony J. Kanai. University of Pittsburgh Department of Pharmacology, Pittsburgh PA 15261, University of Pittsburgh Department of Medicine, Pittsburgh PA 15261, Duke University, Department of Biomedical Engineering, Durham NC 27508
APStracts 5:0087F, 1998.
Nitric oxide (NO) has been implicated in the regulation of the lower urinary tract (LUT). However, the source(s) of NO production in the urinary bladder (UB) has not been determined. Accordingly, we used a porphyrinic microsensor placed on the surface of UB strips in vitro to directly measure endogenous NO production. The afferent neurotoxin, capsaicin, and the mixed [alpha]-[beta]-adrenergic agonist, norepinephrine (NE), both evoked transient (1-3 sec) NO release (range 50 nM-1.4 [mu]M). Adrenergic mediated release was not decreased following denervation of the UB, but was abolished following selective removal of the mucosa. On the other hand, release evoked by capsaicin (range 50-900 nM) was significantly decreased after UB denervation. These data indicate that NE releases NO from UB epithelium and capsaicin releases NO from epithelium as well as nervous tissue in the UB. In light of reports that NO may regulate epithelial integrity and function in other tissues, agonist regulation of a constitutive nitric oxide synthase (NOS) activity in the UB may provide a novel mechanism for modulation of bladder and urothelial function. 

Received 28 October 1997; accepted in final form 23 April 1998.
APS Manuscript Number F342-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 8 May 1998