Ca super(2+) dependency of the release of nitric oxide from non-adrenergic non-cholinergic nerves

The role of Ca super(2+) in nitrergic neurotransmission was studied in the canine ileocolonic junction. The specific N-type voltage-sensitive Ca super(2+) channel blocker omega -conotoxin GVIA (CTX) significantly reduced the electrically-evoked non-adrenergic non-cholinergic (NANC) relaxations, preferentially affecting those of low frequency stimulation, in circular muscle strips of the ileocolonic junction. In contrast, the nerve-mediated NANC-relaxations in response to acetylcholine, gamma -aminobutyric acid, and adenosine 5'-triphosphate as well as the relaxations to nitric oxide (NO) and nitroglycerin remained unaffected. We conclude that the release of NO-R in response to NANC nerve stimulation is Ca super(2+)-dependent. The electrically-evoked release of NO-R results from Ca super(2+) entry through CTX-sensitive N-type voltage-sensitive Ca super(2+) channels, whereas that induced by nicotinic receptor activation involves CTX-insensitive Ca super(2+) channels, different from the L- or N-type.