NITRIC-OXIDE AS NEUROMODULATOR OF SYMPATHETIC TRANSMISSION IN RAT VAS-DEFERENS

1 Electrical field stimulation (EFS) of muscle strips in vitro elicite d a tetrodotoxin (TTX)-sensitive biphasic contractile response consist ing of a phasic component followed by a tonic one. 2 The amplitude of both components of the response was impaired by N-omega-nitro-L-argini ne and potentiated by sodium nitroprusside. Cystamine caused a reducti on in amplitude of both phasic and tonic components of the response to EFS. Neither N-omega-nitro-L-arginine, sodium nitroprusside, nor cyst amine induced changes in the resting muscle tone, or in the contractil e response to exogenous agonists ATP and noradrenaline (NA). 3 The nit ric oxide scavenger, nyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide , induced a reduction in amplitude of both components of the response to EFS. 4 These results reveal a facilitatory prejunctional modulatory role for nitric oxide in sympathetic neurotransmission in rat vas def erens. Endogenous nitric oxide released in the extracellular space is presumed to potentiate neurotransmission by acting at prejunctional le vel via cGMP.