The possible effect of nitric oxide on relaxation and noradrenaline release in the isolated rabbit urethra.
نویسندگان
چکیده
We evaluated the effects of N(omega)-nitro-L-arginine (L-NNA, a nitric oxide (NO) synthase inhibitor) and carboxy-2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (carboxy-PTIO, a NO scavenger) on NO-mediated relaxation and noradrenaline release from adrenergic nerve endings induced by electrical field stimulation in the rabbit urethra. Electrical field stimulation caused frequency-dependent relaxation of rabbit urethral smooth muscles precontracted with phenylephrine. The relaxation responses were significantly inhibited by treatment with L-NNA or carboxy-PTIO. The inhibitory effect of carboxy-PTIO was significantly weaker than that of L-NNA. Electrical field stimulation caused significant noradrenaline release from adrenergic nerve endings in the rabbit urethra. Treatment with carboxy PTIO enhanced electrical field stimulation-induced noradrenaline release, and simultaneous application of L-NNA and carboxy-PTIO did not further enhance noradrenaline release in the rabbit urethra. As carboxy-PTIO reacts only with the free radical NO, the present results suggest that free radical NO and NO-containing compounds are involved in the L-NNA-sensitive nitrergic nerve-mediated relaxation in the rabbit urethra. At the same time free radical NO has a prejunctional action by which it may inhibit noradrenaline release from adrenergic nerves.
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Nitric oxide (NO), previously known as Endothelium-Derived Relaxing Factor (EDRF) is involved in a wide range of physiological and pathophysiological mechanisms. It is synthesized endogenously by the enzymes Nitric Oxide Synthase (NOS) in specialized tissues from its precursor L-arginine, yielding L-citrulline as a byproduct. It is released by a family of isoenzymes, viz., the endothelial (eNOS...
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ورودعنوان ژورنال:
- European journal of pharmacology
دوره 357 2-3 شماره
صفحات -
تاریخ انتشار 1998