Regulation of Monoaminergic Neurons in the Brain through Both Nitiric Oxide and Superoxide Anion

用大鼠主动脉研究了6-硝基肾上腺素的血管活性。6-硝诺啡肽（> 100 μ M）引起内皮完整和剥脱主动脉的剂量依赖性收缩，尽管后者比前者表现出更大的收缩。哌唑嗪（> 3 nM），一种肾上腺素受体拮抗剂，显著减弱6-硝基肾上腺素诱导的收缩，提示肾上腺素受体参与。从利血平预处理大鼠制备的主动脉环显示6-硝基肾上腺素诱导的收缩程度与未处理大鼠相似，表明内源性去甲肾上腺素在6-硝基肾上腺素诱导的收缩中不起作用。6-硝诺啡肽（> 10 μ M）仅在内皮存在的情况下增强去甲肾上腺素诱导的收缩。过氧化氢酶（1200 U/ml）可减弱增强作用。H2 O2（10-300 μ M）仅在内皮完整的大鼠主动脉环中增强去甲肾上腺素诱导的收缩。6-硝诺啡肽明显减弱乙酰胆碱引起的血管舒张。过氧化氢酶阻止6-硝基肾上腺素引起的抑制乙酰胆碱引起的舒张。这些结果表明，6-nitronorepinephrine有一个弱的肾上腺素受体激动剂的属性和内皮依赖性增强6-nitronorepinephrine诱导的收缩介导通过生产H2 O2。

Vasoactivities of 6-nitronorepinephrine were investigated using rat aorta. 6-Nitronorepinephrine (> 100 microM) caused dose-dependent contraction in both endothelium-intact and -denuded aorta, although the latter showed greater contraction than the former. Prazosin (> 3 nM), an alphal-adrenoceptor antagonist, attenuated significantly the 6-nitronorepinephrine-induced contractions, there by suggesting the alphal-adrenoceptor involvement. Aortic rings prepared from reserpine-pretreated rats showed the 6-nitronorepinephrine-induced a contraction to the extent similar to those from untreated rats, suggesting that endogenous norepinephrine does not play a role in the 6-nitronorepinephrine-induced contraction. 6-Nitronorepinephrine (> 10 microM) potentiated norepinephrine-induced contraction only in the presence of endothelium. The augmentation was attenuated by catalase (1200 U/ml). H2O2 (10-300 microM) augmented the norepinephrine-induced contraction only in the endothelium-intact rat aortic rings. 6-Nitronorepinephrine attenuated significantly acetylcholine-induced relaxation. Catalase prevented the 6-nitronorepinephrine-induced inhibition of the acetylcholine-induced relaxation. These results suggest that 6-nitronorepinephrine has a weak alphal-adrenoceptor agonistic property and that the endothelium-dependent potentiation by 6-nitronorepinephrine of the norepinephrine-induced contraction is mediated through production of H2O2.