Vasodilation brake
PDE5 / erection signal
Also searched as PDE5 / erection signal.
The mechanism the entire PDE5-inhibitor class targets. Blocking it does not create the signal — it stops the signal being cleared, which is why arousal is still required for the effect.
In depth
The enzyme that ends the nitric-oxide signal by degrading cGMP. Inhibiting it does not create the erectile signal — it prevents its termination, which is why arousal remains a prerequisite.
What drives it
Blood flow (nitric oxide) reduces it.
cGMP is the substrate PDE5 degrades - the NO/cGMP arm and PDE5 set opposite ends of the same signal. Carried by the vascular and erectile physiology reviews. doi 10.21037/tau-2025-419 · PMC11988752
Cellular aging reduces it.
PDE5 expression rises with vascular aging, shortening the cGMP signal. Carried by the vascular and erectile physiology reviews. doi 10.21037/tau-2025-419 · PMC11988752
What it drives
It reduces Vessel wall muscle.
PDE5 terminates cGMP-mediated smooth-muscle relaxation. Carried by the vascular and erectile physiology reviews. doi 10.21037/tau-2025-419 · PMC11988752
It reduces Sexual function.
The mechanism the PDE5-inhibitor class targets - blocking it prevents the signal being cleared rather than creating it, which is why arousal is still required. Carried by the vascular and erectile physiology reviews. doi 10.21037/tau-2025-419 · PMC11988752
It reduces Vasodilation signal.
10.1038/ncomms8235 — a second way onto the same road, and it does not need the hormone at all. The messenger of this road is destroyed by a specific enzyme, so blocking that enzyme raises the messenger directly: 'the cGMP-mediated browning effect of NPs may underlie the ability of sildenafil (A phosphodiesterase-5 inhibitor) to cause browning' (Mayo Clin Proc s0025-6196(15)00644-8 — An Emerging Role of Natriuretic Peptides). And the road does more than release: 'activation of cGMP-dependent protein kinase through npr-A on adipocytes not only stimulates lipolysis but also activates p38 MAPK, leading to increased expression of UCP-1 and PGC-1α' — it releases fat and turns on the machinery that burns it. One non-ingredient lever is worth knowing: 'circulating levels of ANP and BNP ARE both increased after exposure to cold temperature. Cold exposure increases the expression of NPR-A' — cold raises the hormone and the working receptor at once. doi 10.1038/ncomms8235
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.