Shinozuka K, Kobayashi Y, Shimoura K, Hattori K
Department of Pharmacology, Shimane Medical University, Izumo, Japan.
Eur J Pharmacol. 1992 Nov 3;222(1):113-20. doi: 10.1016/0014-2999(92)90470-o.
The effects of L-NG-nitro arginine (L-NO2Arg), a stereospecific inhibitor of nitric oxide formation, on the responsiveness of rabbit pulmonary artery to transmural electrical stimulation were studied. The contractile response evoked by electrical stimulation at 4 Hz was abolished by tetrodotoxin (10(-7) M) and depressed to approximately 10% by bunazosin (10(-6) M), an alpha 1-antagonist. Pretreatment with L-NO2Arg (10(-5) M) significantly potentiated the response to electrical stimulation without changing the resting tension. D-NO2Arg (10(-5) M) did not show such a potentiating action. In endothelium-denuded arteries, L-NO2Arg did not potentiate the response to electrical stimulation. The effect of L-NO2Arg on endogenous noradrenaline release in response to electrical stimulation was also examined by HPLC with electrochemical detection; L-NO2Arg did not affect noradrenaline release. The contractions induced by exogenous noradrenaline (10(-6)-10(-5) M) were enhanced by L-NO2Arg, but not by D-NO2Arg. These results suggest that the vasoconstriction induced by sympathetic nerve stimulation in the rabbit pulmonary artery is modulated by endogenous nitric oxide or nitric oxide-like substances released from endothelial cells.
研究了一氧化氮生成的立体特异性抑制剂L-NG-硝基精氨酸（L-NO2Arg）对兔肺动脉对跨壁电刺激反应性的影响。4Hz电刺激诱发的收缩反应可被河豚毒素（10^(-7)M）消除，被α1拮抗剂布那唑嗪（10^(-6)M）抑制至约10%。用L-NO2Arg（10^(-5)M）预处理可显著增强对电刺激的反应，而不改变静息张力。D-NO2Arg（10^(-5)M）未表现出这种增强作用。在内皮剥脱的动脉中，L-NO2Arg不能增强对电刺激的反应。还通过高效液相色谱电化学检测研究了L-NO2Arg对电刺激引起的内源性去甲肾上腺素释放的影响；L-NO2Arg不影响去甲肾上腺素的释放。L-NO2Arg可增强外源性去甲肾上腺素（10^(-6)-10^(-5)M）引起的收缩，但D-NO2Arg不能。这些结果表明，兔肺动脉中交感神经刺激诱导的血管收缩受内皮细胞释放的内源性一氧化氮或一氧化氮样物质调节。
