Neurochemical plasticity of nitric oxide synthase isoforms in neurogenic detrusor overactivity after spinal cord injury

Neurochem Res. 2011 Oct;36(10):1903-9. doi: 10.1007/s11064-011-0512-4. Epub 2011 May 28.


Nitric oxide (NO) participates in the neural pathways controlling the lower urinary tract (LUT). Expression of NO synthase (NOS) can be upregulated after spinal cord injury (SCI), and altered NOS activity may participate in resulting LUT dysfunction. To investigate distribution of NOS-immunoreactivity (NOS-IR) in neurons of rats following SCI and the possible effects of NOS inhibitors. Expression of neuronal and inducible NOS-IR in lumbosacral spinal cord was assessed in rats. Cystometry was performed to examine effects of intrathecal injection of NOS inhibitor. There was increased expression of neuronal NOS-IR after trauma. Maximum bladder capacity was increased by neuronal NOS (nNOS) inhibitors. Upregulation of nNOS may facilitate emergence of the spinal micturition reflex following SCI; nNOS inhibitor suppressed SCI-induced urinary incontinence by increasing bladder capacity. Our results indicate manipulation of NO production could help treat LUT dysfunction after SCI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Enzyme Inhibitors / pharmacology
  • Female
  • Humans
  • Injections, Spinal
  • Isoenzymes / metabolism*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Spinal Cord Injuries / complications*
  • Spinal Cord Injuries / enzymology*
  • Spinal Cord Injuries / physiopathology
  • Urinary Bladder / drug effects
  • Urinary Bladder / innervation
  • Urinary Bladder / physiopathology
  • Urinary Bladder, Overactive / enzymology*
  • Urinary Bladder, Overactive / etiology*
  • Urinary Bladder, Overactive / physiopathology
  • Urination / drug effects
  • Urination / physiology


  • Enzyme Inhibitors
  • Isoenzymes
  • Nitric Oxide
  • Nitric Oxide Synthase