Evora Paulo R B, Pearson Paul J, Rodrigues Alfredo José, Viaro Fernanda, Schaff Hartzell V
Laboratório de Função Endotelial, Divisão de Cirurgia Experimental, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.
Arq Bras Cardiol. 2003 Jun;80(6):626-30; 621-5. doi: 10.1590/s0066-782x2003000600005. Epub 2003 Jul 2.
To study the mechanism by which poly-L-arginine mediates endothelium-dependent relaxation.
Vascular segments with and without endothelium were suspended in organ chambers filled with control solution maintained at 37 C and bubbled with 95% O2 / 5% CO2. Used drugs: indomethacin, acetycholine, EGTA, glybenclamide, ouabain, poly-L-arginine, methylene blue, N G-nitro-L-arginine, and verapamil and N G-monomethyl-L-arginine. Prostaglandin F2 and potassium chloride were used to contract the vascular rings.
Poly-L-arginine (10-11 to 10-7 M) induced concentration-dependent relaxation in coronary artery segments with endothelium. The relaxation to poly-L-arginine was attenuated by ouabain, but was unaffected by glybenclamide. L-NOARG and oxyhemoglobin caused attenuation, but did not abolish this relaxation. Also, the relaxations was unaffected by methylene blue, verapamil, or the presence of a calcium-free bathing medium. The endothelium-dependent to poly-L-arginine relaxation was abolished only in vessels contracted with potassium chloride (40 mM) in the presence of L-NOARG and indomethacin.
These experiments indicate that poly-L-arginine induces relaxation independent of nitric oxide.
研究聚-L-精氨酸介导内皮依赖性舒张的机制。
将有内皮和无内皮的血管段悬挂于充满对照溶液的器官浴槽中，保持在37℃，用95%O₂/5%CO₂鼓泡。使用的药物：吲哚美辛、乙酰胆碱、乙二醇双乙醚二胺四乙酸（EGTA）、格列本脲、哇巴因、聚-L-精氨酸、亚甲蓝、N-硝基-L-精氨酸、维拉帕米和N-单甲基-L-精氨酸。用前列腺素F2和氯化钾使血管环收缩。
聚-L-精氨酸（10⁻¹¹至10⁻⁷M）在有内皮的冠状动脉段诱导浓度依赖性舒张。哇巴因减弱了对聚-L-精氨酸的舒张反应，但格列本脲无影响。L-硝基精氨酸（L-NOARG）和氧合血红蛋白引起舒张减弱，但并未消除这种舒张。此外，亚甲蓝、维拉帕米或无钙浴液的存在对舒张无影响。仅在L-NOARG和吲哚美辛存在下用氯化钾（40mM）收缩的血管中，聚-L-精氨酸的内皮依赖性舒张被消除。
这些实验表明聚-L-精氨酸诱导的舒张不依赖于一氧化氮。
