The nitric oxide pathway behind an erection
An erection is fundamentally a vascular event. Sexual stimulation triggers release of nitric oxide in the penile tissue, which raises levels of cyclic GMP, relaxing the smooth muscle of the arteries and the spongy erectile tissue. Blood inflow increases, the tissue engorges, and the resulting pressure compresses the outflow veins to maintain rigidity. The enzyme PDE5 later breaks down cyclic GMP, allowing the erection to subside.
PDE5 inhibitors work by slowing that breakdown, prolonging the cyclic GMP signal. They do not create an erection on their own; they amplify the natural response and still require sexual stimulation and an intact nitric oxide pathway.
Sorting the underlying causes
Erectile dysfunction is commonly grouped by mechanism: vascular (impaired blood flow), neurogenic (nerve signalling, as after pelvic surgery or in diabetes), psychogenic (anxiety, depression, relationship factors), and hormonal (notably low testosterone). These often overlap, and vascular causes become more common with age and cardiovascular risk.
This is general educational information, not medical advice. Medications including PDE5 inhibitors can interact dangerously with nitrates and are not suitable for everyone, so any treatment should be guided by a clinician.