Wake Forest Institute for Regenerative Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston Salem, NC 27157, USA.
Pharmacol Rev. 2011 Dec;63(4):811-59. doi: 10.1124/pr.111.004515. Epub 2011 Aug 31.
Erection is basically a spinal reflex that can be initiated by recruitment of penile afferents, both autonomic and somatic, and supraspinal influences from visual, olfactory, and imaginary stimuli. Several central transmitters are involved in the erectile control. Dopamine, acetylcholine, nitric oxide (NO), and peptides, such as oxytocin and adrenocorticotropin/α-melanocyte-stimulating hormone, have a facilitatory role, whereas serotonin may be either facilitatory or inhibitory, and enkephalins are inhibitory. The balance between contractant and relaxant factors controls the degree of contraction of the smooth muscle of the corpora cavernosa (CC) and determines the functional state of the penis. Noradrenaline contracts both CC and penile vessels via stimulation of α₁-adrenoceptors. Neurogenic NO is considered the most important factor for relaxation of penile vessels and CC. The role of other mediators, released from nerves or endothelium, has not been definitely established. Erectile dysfunction (ED), defined as the "inability to achieve or maintain an erection adequate for sexual satisfaction," may have multiple causes and can be classified as psychogenic, vasculogenic or organic, neurologic, and endocrinologic. Many patients with ED respond well to the pharmacological treatments that are currently available, but there are still groups of patients in whom the response is unsatisfactory. The drugs used are able to substitute, partially or completely, the malfunctioning endogenous mechanisms that control penile erection. Most drugs have a direct action on penile tissue facilitating penile smooth muscle relaxation, including oral phosphodiesterase inhibitors and intracavernosal injections of prostaglandin E₁. Irrespective of the underlying cause, these drugs are effective in the majority of cases. Drugs with a central site of action have so far not been very successful. There is a need for therapeutic alternatives. This requires identification of new therapeutic targets and design of new approaches. Research in the field is expanding, and several promising new targets for future drugs have been identified.
勃起基本上是一种脊柱反射，可以通过募集阴茎传入神经（自主和躯体传入神经）以及来自视觉、嗅觉和想象刺激的中枢传入神经来启动。几种中枢递质参与勃起的控制。多巴胺、乙酰胆碱、一氧化氮（NO）和肽类，如催产素和促肾上腺皮质激素/α-黑色素细胞刺激素，具有促进作用，而 5-羟色胺可能具有促进或抑制作用，而脑啡肽具有抑制作用。收缩性和松弛性因素之间的平衡控制海绵体平滑肌的收缩程度，并决定阴茎的功能状态。去甲肾上腺素通过刺激α₁-肾上腺素受体收缩 CC 和阴茎血管。神经源性 NO 被认为是阴茎血管和 CC 松弛的最重要因素。从神经或内皮释放的其他介质的作用尚未得到明确证实。勃起功能障碍（ED）定义为“无法获得或维持足以获得性满足的勃起”，可能有多种原因，并可分为心理性、血管性或器质性、神经性和内分泌性。许多 ED 患者对目前可用的药物治疗反应良好，但仍有一些患者的反应不理想。所用药物能够部分或完全替代控制阴茎勃起的内源性机制的功能障碍。大多数药物对阴茎组织有直接作用，促进阴茎平滑肌松弛，包括口服磷酸二酯酶抑制剂和前列腺素 E₁的海绵体内注射。无论潜在原因如何，这些药物在大多数情况下都有效。具有中枢作用的药物到目前为止并不非常成功。需要有治疗的替代方法。这需要确定新的治疗靶点和设计新的方法。该领域的研究正在扩展，已经确定了几个有前途的未来药物的新治疗靶点。
