Upregulation of nicotinamide adenine dinucleotide phosphate-diaphorase reactivity in the ventral horn motoneurons of lumbosacral spinal cord after urethral obstruction in the guinea pig.

The role of nitric oxide (NO) in pathophysiology of urethral obstruction in male guinea pig was investigated by using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. In normal and sham-operated control animals, NADPH-d reactivity in the ventral horn motoneurons at L5-L6 and S1-S2 segments of spinal cord was barely detectable or virtually absent. In animals receiving urethral ligation and killed at 6 h after operation, NADPH-d reactivity in the ventral horn motoneurons was comparable to that of control animals. At 12 h, NADPH-d reactivity in the same cells began evident and was markedly enhanced in animals killed at 24 and 48 h. In order to verify whether the increased NADPH-d reactivity was linked to neuronal death, some sections of the lumbosacral spinal cord from urethral obstructed animals were stained in Nissl staining. There was no sign of cell death or atrophy of the ventral horn neurons. Present results suggest the plasticity of NADPH-d in ventral horn neurons which is readily upregulated by urethral ligation. The enhanced NADPH-d reactivity would imply increased nitric oxide synthase (NOS) activity and consequently generation of higher levels of NO in ventral horn neurons. Such alteration maybe involved in distension-induced urethral relaxation in the external urethral sphincter following urethral ligation.