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1 Department of Urology and Reproductive Medicine and 2 Department of Molecular Design, Institute of Biomaterials and Bioengineering, Graduate School, Tokyo Medical and Dental University, Tokyo 101 - 0062, Japan
We examined whether endogenous inhibitors of nitric oxide (NO) synthesis are involved in the impaired cavernosal relaxation with ischemia in rabbits. Two weeks after cavernosal ischemia caused by partial vessel occlusion, endothelium-dependent and electrical field stimulation (EFS)-induced neurogenic NO-mediated relaxations, but not sodium nitroprusside (SNP)-induced relaxation, were significantly impaired in the isolated corpus cavernosum. The Ca2+-dependent NO synthase (NOS) activity and the basal and stimulated cGMP productions with carbachol or EFS were significantly decreased after ischemia. Supplementation of excess L-arginine partially recovered both of the impaired relaxations. The contents of NG-monomethyl-L-arginine (L-NMMA) and asymmetric NG, NG-dimethyl-L-arginine (ADMA) but not L-arginine and symmetric NG,N'G-dimethyl-L-arginine (SDMA) were increased in the cavernosal tissues after ischemia. Authentic L-NMMA and ADMA but not SDMA concentration dependently inhibited both relaxations without affecting the relaxation produced by SNP in the control. Excess L-arginine abolished the inhibition with L-NMMA and ADMA. These results suggest that the impaired NO-mediated cavernosal relaxations after ischemia are closely related to the decreased NOS activity and the increased accumulation of L-NMMA and ADMA.
asymmetric NG,NG-dimethyl-L-arginine; L-arginine; NG-monomethyl-L-arginine; corpus cavernosum
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