Nitric oxide synthase, which catalyzes nitric oxide (NO) production, has been localized in nerves supplying the mammalian vas deferens and, in spite of contradictory reports, nitrergic modulation by NO seems to be implicated in the adrenergic neurotransmission. In the present work, direct responses to noradrenaline (NA) were obtained from isolated unstimulated vasa deferential and adrenergic neurotransmission was studied in electrically stimulated preparations challenged with acetylcholine (ACh), which stimulates prejunctional hetero-receptors that enhance neurotransmission release from sympathetic nerve terminals. Pretreatment with L-arginine (L-ARG) significantly enhanced the contractile response of unstimulated preparations to NA, an effect which was abolished by pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), suggesting than NO release may modulate postjunctional effector sensitivity. Electrical stimulation elicited a twitch response, which was significantly reduced by L-ARG pretreatment. The addition of ACh during electrical stimulation enhanced the twitch response, which was significantly potentiated by L-ARG, suggesting a facilitation of adrenergic neurotransmission. Pretreatment with L-NAME abolished the potentiation induced by L-ARG. The overall results suggest that NO released in the extracellular space exerts a facilitatory modulation of adrenergic neurotransmission and probably modulates the effector sensitivity.
|Number of pages||6|
|Journal||Pharmacology Reviews and Communications|
|Publication status||Published - 2001|
- Nitric oxide
- Vas deferens
ASJC Scopus subject areas