Alterations of NOS, arginase, and DDAH protein expression in rabbit cavernous tissue after administration of cigarette smoke extract

摘要: Cigarette smoking is an independent risk factor for vasculogenic erectile dysfunction (ED). Nitric oxide (NO) has been demonstrated to be the principal mediator of cavernous smooth muscle relaxation and penile erection. Therefore, we examined whether or not enzyme activities factors involved in NO generation pathway are affected rabbit corpus cavernosum after administration nicotine- tar-free cigarette smoke extract (CSE). CSE was prepared by bubbling a stream into phosphate-buffered saline. injected subcutaneously adult male rabbits once day 5 wk. In group, significantly decreased cyclic GMP production as marker associated with attenuated overall nitric synthase (NOS) activity, enhanced arginase accumulation endogenous NOS inhibitors such monomethylarginine (MMA) asymmetric dimethylarginine (ADMA), dimethylaminohydrolase (DDAH) activity metabolizing inhibitors. Neuronal (nNOS) DDAH I protein expression were without altering endothelial expression, while upregulated. These results suggest that impaired would result from blunted which possibly brought about downregulation nNOS protein, inhibitors, together upregulation tissue. The due CSE. alterations may relevant induction following