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How to use Rogaine topical

Read and follow all directions on the merchandise package before exploitation of this product. If you're unsure concerning any of the data, consult your doctor or pill pusher.


Clean and dry the scalp space before applying the medication. you will apply this product to damp hair. To use the answer, fill the device or the applicator with one ml = 1cubic centimeter of medication (to the one cubic centimeter line), or use twenty drops. half your hair within the space of dilution and apply the answer equally to the affected space of the scalp. Gently rub in. enable the solution to dry fully before the use of alternative merchandise (gels, mousse...) or before getting to bed.

To use the froth, rinse your hands in cold water and dry well. Apply concerning 1/2 containerful of froth to the scalp and rub in gently. permit the froth to dry fully before styling or about to bed.

If scalp irritation could be a downside, you will have to avoid treatment with minoxidil on identical days that you simply have your hair coloured or with chemicals treated (ex: permed).

Do not use on alternative elements of the body unless directed by your doctor. don't use on skin that's red, painful, irritated, scraped, cut, or infected. Wash hands completely when application. Avoid obtaining the medication in your eyes. If this happens, rinse your eyes with massive amounts of cool water.

Do not use this medication a lot of usually, apply additional of it than as directed, or apply it to associate irritated or sunburnt scalp. Doing thus will cause the drug to be absorbed into your body and lead to serious facet effects. This product could contain alcohol and might be irritating and drying to the scalp. raise your doctor or health professional or pharmacist the way to use this product safely.

It takes time for hair to grow again. the majority of people have to use this medication frequently for four months to check profit. This medication should be used unceasingly to keep up hair growth. If your condition doesn't improve or worsens when the use of this medication for four to six months, or if you're thinking that you will have a significant medical side effects, tell your doctor.


bay 6 months of minoxidil for 28$ 

Mechanism of action of minoxidil

Since these initial studies, much research has been done to identify exactly how the topical application of minoxidil can lead to increased hair growth. One important hypothesis is based on its vasodilatory properties. Diazoxide is another antihypertensive potassium channel opener which increases blood flow and is reputed to increase hair growth. Laser Doppler velocimetry studies showed an increase in cutaneous blood flow after applying 1%, 3%, and 5% minoxidil solutions to the scalps of 16 balding men.16 All three groups showed increases compared to a control group, and the 5% group showed the greatest increase. A significant increase in blood flow occurred as soon as 15 minutes after application, and lasted for up to an hour. The role of minoxidil in angiogenesis is further supported by evidence that it upregulates the expression of vascular endothelial growth factor mRNA in human hair dermal papilla cells.

Minoxidil sulfate is the active metabolite that stimulates hair follicles. The conversion of minoxidil to minoxidil sulfate is catalyzed by sulphotransferase enzymes, which exist in the scalp. In scalp skin of the stump-tailed macaque, this enzyme has been localized mainly to the hair follicle, which contains 50% to 85% of the enzyme (versus 10-20% in the epidermis and dermis). Immunolocalization studies of minoxidil sulphotransferase demonstrated that the lower outer root sheath is the most likely site of conversion of minoxidil to its sulfated form. Just as is the case with dihydrotestosterone (DHT), there are interindividual variations in scalp sulphotransferase levels. Patients with a better response to topical minoxidil were found to have a greater level of enzyme activity.

Cultures of human epidermal cells treated with minoxidil have been shown to survive longer than control cultures. Minoxidil slows the senescence of keratinocytes and reduces the rate at which cells are lost from the germinative pool. This is similar to what has been found with epidermal growth factor. Minoxidil has been shown to increase the proliferation of dermal papilla cells of the human hair follicle. Specifically, minoxidil increased levels of Erk and Akt phosphorylation, with an increased ratio of Bcl-2/Bax, prolonging anagen and preventing cell death with antiapoptotic effects. This same study found that minoxidil elongated individual hair follicles in organ culture.

Minoxidil may also enhance cell proliferation. The uptake of tritiated minoxidil and its conversion to minoxidil sulfate has been found to be relatively higher in the hair follicles than in the epidermis and dermis. This group also found that minoxidil caused the enhancement of DNA synthesis in the follicular and perifollicular cells but not in the epidermal keratinocytes. Another study showed a marked dose-dependent second peak of DNA synthesis 8 to 10 days later in epidermal cells cultured with minoxidil. There were two morphologically distinct cell types, suggesting that minoxidil can affect epidermal cells in culture by altering their growth pattern and phenotypic appearance.

Whether the minoxidil indeed prolongs anagen or simply shortens telogen is still a matter of debate. It has been shown to shorten the length of telogen phase in the follicular cycle of rats but did not prolong the anagen phase. Rather, there was found to be a premature entry of resting hair follicles back into the anagen stage, with an increased rate of DNA synthesis during the anagen stage. However, another study in balding stump-tailed macaques found that treatment with minoxidil increased the proportion of hair follicles in anagen, reduced the number of telogen follicles, and increased the follicle size overall. This suggests at least a relative shift chronologically from telogen to anagen. Abell supported the finding of increased anagen/telogen ratios after 12 months of minoxidil treatment in balding men. However, the main finding was an increase in mean hair diameter, which was evident at 4 months. Other histologic studies also demonstrated an increase in the shaft diameter from 0.029 mm at baseline to 0.043 mm at 12 weeks and 0.042 mm at 24 weeks.

Lastly, it is possible that minoxidil plays an immunoregulatory role in the hair follicle. In vitro studies demonstrate that minoxidil had a suppressive effect on normal human T-lymphocytes in vitro. This may explain minoxidil’s reported efficacy in treating some patients with AA.  This is supported by histologic findings of a reduced perifollicular infiltrate.  There is also evidence that minoxidil can selectively inhibit prostacyclin production by cells in culture. Somewhat like aspirin, minoxidil has been found to prevent the aggregation of platelets by causing a reduction in the synthesis of prostaglandin E2 and thromboxane B2.36 This inhibitory effect on the cyclooxygenase enzyme awaits further study. Regardless of its exact mechanism of action, there is sound histologic and clinical evidence that minoxidil works. A complete list of proposed mechanisms is provided in Table below.


Minoxidil: proposed mechanisms of action
_______________________________
Vasodilatory properties
______________________________
Angiogenic properties
______________________________
Enhanced cell proliferation and DNA synthesis
______________________________
Potassium channel opener
______________________________
Antiandrogen effects
______________________________
Suppression of collagen synthesis
______________________________
Immunosuppressive effects

the discovry of minoxidil molecule

The use of minoxidil for hair loss has an important history. It was first used during the 1970 as an oral medication for refractory cases of high blood pressure. The molecule is a piperidinopyrimidine derivative, with the chemical structure 2,6-diamino- 4-piperidinopyrimidine 1-oxide .


 It serves as an arteriolar vasodilator, acting specifically to open potassium channels. It also was found to have a side effect of hypertrichosis. , it was found to cause unwanted hair growth in 24% to 100%  of patients. Hypertrichosis was also noted in 5 out of 6 patients treated with minoxidil.  hypertrichosis is observed in a high frequency and at lower doses in women than in men No endocrine abnormalities have been associated, but darkening of the skin and the coarsening of facial features have been reported from long-term oral use.

Hypertrichosis caused by minoxidil was not reported in the dermatology literature until 1979 That same year, the oral tablet form, Loniten (Pharmacia & Upjohn, Bridgewater, NJ), was approved by the FDA for hypertension. Other dermatologists quickly took note in considering it for use in treating different forms of hair loss. Zapacosta  noted a reversal of androgenetic alopecia (AGA) in a patient receiving oral minoxidil. However, there were limitations to using the oral formulation, because it could cause an unsafe drop in blood pressure. Patients also experienced side effects of severe water retention and weight gain, often requiring concomitant treatment with a diuretic.

Therefore, several researchers tested its use as a topical formulation for hair loss. Two controlled trials using 1% topical minoxidil for alopecia areata (AA) demonstrated cosmetically acceptable regrowth in approximately half of patients. In 1984, topical minoxidil was used for the treatment of AGA. Five patients with AGA and 10 with AA were randomized to 1% or 5% topical minoxidil or placebo. Regrowth was seen in the 3 patients with AGA who were given the 5% solution, suggesting a clinical dose response. Blood levels of minoxidil were 0.5, 2.0, and 4.5 ng/mL 2 hours after application to the scalp. None of the patients with AA regrew hair, despite comparable blood levels.