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Noradrenergic‐nitrergic interactions in the rat anococcygeus muscle: evidence for postjunctional modulation by nitric oxide

1 The distribution of NADPH‐diaphorase positive and catecholamine‐containing nerve structures, and functional noradrenergic‐nitrergic interactions, were studied in the rat anococcygeus muscle. 2 The morphological findings demonstrated NADPH‐diaphorase positive neurones mostly as aggregates in intramural ganglia, nerve tracts and few single nerve fibres forming plexus‐like structures. 3 The nitric oxide synthase inhibitor NG‐nitro‐l‐arginine (l‐NOARG) inhibited concentration‐dependently the nitrergic relaxation, an effect reversed by l‐arginine. The drug had dual effects on noradrenergic contractile responses: at lower concentrations (0.1–10 μm) it decreased the amplitude of contractions and this was not affected by l‐arginine; higher concentrations (50–500 μm) potentiated the contractions, an effect that was prevented by l‐arginine. 4 The electron acceptor, nitro blue tetrazolium (NBT) produced a rapid inhibition of the noradrenergic contractile responses (EC50 0.178 ± 0.041 μm). The drug decreased the tone of the preparations. However, it potentiated concentration‐dependently the nitrergic relaxations. 5 NBT (1 μm) had no significant effect on the relaxations induced by exogenously applied nitric oxide (NO)‐donor sodium nitroprusside (SNP, 0.01–50 μm). However, the effect of NBT (0.1–10 μm) on the electrically induced relaxation was significantly decreased by l‐NOARG (10 and 50 μm). The inhibition was of a non‐competitive type. 6 Neither l‐NOARG (100 μm) nor NBT (1 μm) had any effect on the spontaneous or electrically‐induced release of 3H‐radioactivity from the tissues preincubated in [3H]‐noradrenaline. 7 It is concluded that l‐arginine‐NO pathway can modulate noradrenergic transmission in the rat anococcygeus muscle at postjunctional, but not prejunctional site(s).