Characterization of nitrergic neurotransmission during short‐and long‐term electrical stimulation of the rabbit anococcygeus muscle

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Abstract
1 Isolated preparations of rabbit anococcygeus muscle were exposed to electrical field stimulation (EFS; 50V, 0.3 ms duration, 0.08–40 Hz) for periods of 1–60 s (short-term EFS) or 10 min-2 h (long-term EFS). 2 Both short- and long-term EFS caused a contractile response which was enhanced by the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine (L-NOARG), showing that it is modulated by endogenous NO. 3 In preparations treated with scopolamine and guanethidine and in which a constrictor tone was induced by histamine, both short- and long-term EFS resulted in relaxation of the tissue. 4 Such relaxations were reversed by tetrodotoxin (TTX), ω-conotoxin, inhibitors of NO synthase and the NO scavenger, oxyhaemoglobin, indicating that they are neuronal in origin and nitrergic in nature. 5 The relaxations to long-term EFS persisted for the duration of the stimulation and were associated with sustained release of oxidation products of NO (NOx). The EFS-induced release of NOx was decreased by N-iminoethyl-L-ornithine (L-NIO), an inhibitor of NO synthase, and by TTX. 6 Inhibitors of NO synthase, in addition, increased the basal tone of the tissue and reduced the basal output of NOx. The basal output of NOx was also reduced by TTX. 7 Long-term EFS which induces ∼ 50% of the maximum relaxation could be enhanced by addition of L-, but not D-, arginine to the perfusion medium. 8 These data show that there is a continuous basal release of NO from nitrergic nerve terminals which maintains a relaxant tone in the rabbit anococcygeus muscle. 9 In addition, NO is released during short- and long-term EFS which further relaxes the preparation and modulates sympathetic transmission. Activation of the L-arginine: NO pathway for periods up to 2 h does not exhaust nitrergic transmission in any appreciable way.