The mechanism by which minoxidil promotes hair growth is not fully understood. Hypothetically, by widening blood vessels and opening potassium channels, it allows more oxygen, blood, and nutrients to the follicles. This may cause follicles in the telogen phase to shed, which are then replaced by thicker hairs in a new anagen phase. Minoxidil is a prodrug that is converted by sulfation via the sulfotransferase enzyme SULT1A1 to its active form, minoxidil sulfate. Several studies demonstrated that the activity of sulfotransferase in hair follicles predict minoxidil response in the treatment of hair loss. In order for a significant amount of hair to pass through the growth phase and become healthy, it takes a long time, so the effect of treatment is noticeable after about 4 months of using minoxidil.
Minoxidil contains nitric oxide (II) [NO] – the chemical functional group of nitrogen and can interact with the nitrogen oxide receptors, changing their state. Minoxidil is a potassium channel opener, causing hyperpolarization of cell membranes.
Minoxidil stimulates the hair follicles and hair growth, but does not affect the causes of androgenetic alopecia (hair loss) development, which lie at the gene level and consist in the damaging effect on the hair follicles of the active form of the male sex hormone testosterone-dihydrotestosterone, formed under the influence of the enzyme 5-alpha -reductase, located in the hair follicles.
With the termination of minoxidil treatment, the action of dihydrotestosterone and 5-alpha-reductase on the hair follicle continues. Dihydrotestosterone, penetrating into the cells of the follicles, causes their dystrophy and, accordingly, the dystrophy of the hair produced by them. The hair on the head remains, but they become thin, short and colorless (fleecy hair).
After 10-12 years after the appearance of the alopecia, the follicles are overgrown with a connective tissue, and they can no longer produce even fleece hair.