What is the mechanism of erection?

Mechanism of Penile Erection

Penile erection is the result of a complex neurovascular process involving the coordinated interaction between vascular, neurologic, hormonal, and psychological systems, with nitric oxide (NO) playing the central role in mediating smooth muscle relaxation and increased blood flow into the corpus cavernosum. 1

Physiological Cascade of Erection

Neural Initiation

• Erection begins as a spinal reflex that can be triggered by:
  • Recruitment of penile afferents (both autonomic and somatic)
  • Supraspinal influences from visual, olfactory, and imaginary stimuli 2
  • Central neurotransmitters involved include dopamine, acetylcholine, nitric oxide, and peptides (oxytocin) which have facilitatory roles 2

Vascular Mechanism

1. Nitric Oxide Release:

   • Sexual stimulation triggers release of NO from nerve terminals and endothelial cells 3
   • NO is the most important mediator for relaxation of penile vessels and corpus cavernosum 2

2. cGMP Pathway Activation:

   • NO stimulates the synthesis of cyclic guanosine monophosphate (cGMP) in smooth muscle cells
   • cGMP causes smooth muscle relaxation in the corpus cavernosum 3

3. Arterial Dilation and Venous Compression:

   • Relaxation of penile arteries increases blood flow into the corpus cavernosum
   • The increased blood volume in the corpus cavernosum compresses the venous outflow
   • This creates a hydraulic effect that maintains the erection 1, 4

Key Anatomical Components

Vascular Structures

• Arterial System: Penile arteries dilate during erection, increasing blood flow
• Venous System: Venous outflow is reduced through compression of subtunical venules
• Corpus Cavernosum: Specialized erectile tissue that fills with blood during erection 4

Neural Control

• Parasympathetic System: Mediates erection through NO release
• Sympathetic System: Maintains penile flaccidity through noradrenaline release (via α₁-adrenoceptors) 2
• Somatic Nerves: Control pelvic floor muscles that contribute to rigidity

Molecular Mechanisms

Nitric Oxide Pathway

1. NO is released from nerve terminals and endothelial cells
2. NO activates guanylyl cyclase, increasing cGMP production
3. cGMP activates protein kinase G
4. This leads to decreased intracellular calcium and smooth muscle relaxation 3, 5

PDE5 Role

• Phosphodiesterase type 5 (PDE5) normally breaks down cGMP
• PDE5 inhibitors (like sildenafil, tadalafil) block this breakdown
• This prolongs and enhances the NO-mediated smooth muscle relaxation 3, 6

Hormonal Influences

• Testosterone plays a permissive role in erectile function
• Low testosterone levels can impair erectile function through decreased NO production 1
• Other hormonal disorders (thyroid dysfunction, hyperprolactinemia) can also affect erectile function 1

Supraspinal Control

• Multiple brain regions are involved in erectile control:
  • Limbic system: Processes sexual arousal
  • Hypothalamus: Integrates autonomic responses
  • Brainstem: Coordinates cardiovascular responses during sexual activity 7
• These centers modulate the spinal reflexes through descending pathways

Clinical Implications

• Understanding this mechanism has led to targeted therapies for erectile dysfunction
• PDE5 inhibitors work by enhancing the NO-cGMP pathway
• Other treatments target different parts of this mechanism (intracavernosal injections, vacuum devices) 1
• Cardiovascular disease and diabetes often cause ED by impairing endothelial function and NO production 1

The balance between contractile factors (primarily noradrenaline) and relaxant factors (primarily NO) determines the functional state of the penis. When relaxation predominates, erection occurs; when contraction predominates, the penis remains flaccid or returns to the flaccid state 2.