Burnett A L
Department of Urology, The Johns Hopkins Hospital, Baltimore, Maryland 21287-2411, USA.
Int J Impot Res. 2004 Jun;16 Suppl 1:S15-9. doi: 10.1038/sj.ijir.3901209.
Nitric oxide (NO) is a physiologic signal essential to penile erection, and disorders that reduce NO synthesis or release in the erectile tissue are commonly associated with erectile dysfunction. NO synthase (NOS) catalyzes production of NO from L-arginine. While both constitutively expressed neuronal NOS (nNOS) and endothelial NOS (eNOS) isoforms mediate penile erection, nNOS is widely perceived to predominate in this role. Demonstration that blood-flow-dependent generation of NO involves phosphorylative activation of penile eNOS challenges conventional understanding of NO-dependent erectile mechanisms. Regulation of erectile function may not be mediated exclusively by neurally derived NO: Blood-flow-induced fluid shear stress in the penile vasculature stimulates phosphatidyl-inositol 3-kinase to phosphorylate protein kinase B, which in turn phosphorylates eNOS to generate NO. Thus, nNOS may initiate cavernosal tissue relaxation, while activated eNOS may facilitate attainment and maintenance of full erection.
一氧化氮（NO）是阴茎勃起所必需的生理信号，而导致勃起组织中NO合成或释放减少的疾病通常与勃起功能障碍相关。一氧化氮合酶（NOS）催化由L-精氨酸生成NO。虽然组成型表达的神经元型NOS（nNOS）和内皮型NOS（eNOS）同工型均介导阴茎勃起，但人们普遍认为nNOS在这一过程中起主要作用。有证据表明，血流依赖性的NO生成涉及阴茎eNOS的磷酸化激活，这对传统的NO依赖性勃起机制的理解提出了挑战。勃起功能的调节可能并非仅由神经源性NO介导：阴茎血管系统中血流诱导的流体剪切应力刺激磷脂酰肌醇3激酶使蛋白激酶B磷酸化，进而使eNOS磷酸化以生成NO。因此，nNOS可能启动海绵体组织松弛，而激活的eNOS可能促进完全勃起的实现和维持。
