PubMed1996
PURPOSE: Nitric oxide (NO) is known to have an important transmitter function at peripheral synapses in the urogenital tract and has also been implicated in the transmission of nociceptive information in the spinal cord. The present study evaluated the role of NO in the central micturition reflex pathway. MATERIALS AND METHODS: We examined the effect of N-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, on micturition reflexes induced by continuous infusion of saline or 0.1% acetic acid (a noxious stimulus) into the bladder in urethane-anesthetized female rats. Bladder and external urethral sphincter function were monitored with a continuous cystometrogram (CMG) and electromyography (EMG). RESULTS: Intrathecal injection of L-NAME (0.01 to 1 mumol.) did not significantly change the CMG or sphincter EMG during saline infusion. Infusion of acetic acid decreased the intercontraction interval (ICI), indicating a decrease in the volume threshold for inducing micturition. Subsequent intrathecal administration of L-NAME partially reversed the decreased ICI in a dose-dependent manner, but did not change the amplitude of bladder contractions: 0.01, 0.1 and 1 mumol. of L-NAME produced increases of 25%, 31% and 56% in the ICI. D-NAME, the inactive stereoisomer had no effect. This effect of L-NAME was reversed by injection of L-arginine (2 mumol. intrathecally) which, by itself, did not alter ICI during saline infusion or acetic acid infusion. CONCLUSIONS: These results indicate that: (1) spinal NO containing pathways do not play a role in the normal micturition reflex, (2) NO is involved at the spinal level in the facilitation of the micturition reflex by nociceptive bladder afferents activated by noxious chemical irritation of the bladder.