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使用合成代谢类固醇诺龙进行长期治疗会抑制兔主动脉的血管舒张反应。

Chronic treatment with the anabolic steroid, nandrolone, inhibits vasodilator responses in rabbit aorta.

作者信息

Ferrer M, Encabo A, Marín J, Balfagón G

机构信息

Departmento of Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.

出版信息

Eur J Pharmacol. 1994 Feb 3;252(2):233-41. doi: 10.1016/0014-2999(94)90602-5.

DOI:10.1016/0014-2999(94)90602-5
PMID:7908882
Abstract

The effect of chronic treatment of rabbits for 4, 8 and 12 weeks with the anabolic steroid, nandrolone, on vasodilator responses was studied in segments of different arteries. The treatment abolished endothelium-dependent relaxation caused by acetylcholine and the Ca(2+)-ionophore, A23187, in thoracic aorta, and reduced endothelium-independent relaxations induced by exogenous nitric oxide (NO) or sodium nitroprusside. The inhibitor of NO synthesis, NG-monomethyl-L-arginine, abolished vasodilator responses to acetylcholine and A23187. In contrast, relaxation induced by acetylcholine, NO or sodium nitroprusside in mesenteric and femoral arteries was unaltered by nandrolone treatment. Bioassay experiments using donor segments and endothelium-denuded bioassay rings from thoracic aorta show that acetylcholine, applied either through control or treated (12 weeks) donor segments, produced similar relaxation in bioassay rings from control rabbits, but this relaxation was markedly reduced in rings from treated rabbits. The increases of cyclic GMP levels induced by acetylcholine or sodium nitroprusside in segments from thoracic aorta were abolished by nandrolone treatment. These results suggest that the treatment with nandrolone reduces NO-mediated relaxation only in thoracic aorta by inhibition of guanylate cyclase, endothelial NO production and vasodilator machinery being unaltered.

摘要

研究了用合成代谢类固醇诺龙对家兔进行4周、8周和12周长期治疗后,其对不同动脉段血管舒张反应的影响。该治疗消除了胸主动脉中由乙酰胆碱和钙离子载体A23187引起的内皮依赖性舒张,并降低了外源性一氧化氮(NO)或硝普钠诱导的非内皮依赖性舒张。NO合成抑制剂NG-单甲基-L-精氨酸消除了对乙酰胆碱和A23187的血管舒张反应。相比之下,诺龙治疗并未改变肠系膜动脉和股动脉中由乙酰胆碱、NO或硝普钠诱导的舒张。使用胸主动脉的供体段和去内皮生物测定环进行的生物测定实验表明,通过对照或经处理(12周)的供体段施加乙酰胆碱,在对照家兔的生物测定环中产生相似的舒张,但在经处理家兔的环中这种舒张明显减弱。诺龙治疗消除了胸主动脉段中由乙酰胆碱或硝普钠诱导的环磷酸鸟苷水平的升高。这些结果表明,诺龙治疗仅通过抑制鸟苷酸环化酶降低胸主动脉中NO介导的舒张,而内皮NO生成和血管舒张机制未改变。

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