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一氧化氮的促勃起作用能被水解环磷酸鸟苷为失活的鸟苷酸的5型磷酸二酯酶(PDE5)减弱PDE5的上调可促进勃起功能障碍(ED)。有证据表明同型半胱氨酸和铜相互作用可促进ED,对海绵体血管平滑肌细胞(CVSMCs)中PDE5表达的作用进行了研究。对来源于烟酰胺腺嘌呤二核苷酸磷酸氧化酶的超
Nitric oxide promotes erectile dysfunction (ED) by eliciting that PDE5 is upregulated by guanosine monophosphate type 5 phosphodiesterase (PDE5), which hydrolyzes cyclic guanosine monophosphate. There is evidence that homocysteine-copper interaction promotes ED and the effect of PDE5 expression in cavernous vascular smooth muscle cells (CVSMCs) has been investigated. On the derived from nicotinamide adenine dinucleotide phosphate oxidase super