Minoxidil

Minoxidil is an antihypertensive vasodilator medication.

Chronic Treatment with Minoxidil Induces Elastic Fiber Neosynthesis and Functional Improvement in the Aorta of Aged Mice.[Pubmed:28056723]

Rejuvenation Res. 2017 Jun;20(3):218-230.

Normal arterial aging processes involve vascular cell dysfunction associated with wall stiffening, the latter being due to progressive elastin and elastic fiber degradation, and elastin and collagen cross-linking by advanced glycation end products (AGEs). These processes progressively lead to cardiovascular dysfunction during aging. Elastin is only synthesized during late gestation and childhood, and further degradation occurring throughout adulthood cannot be physiologically compensated by replacement of altered material. However, the ATP-dependent K(+) channel opener Minoxidil has been shown to stimulate elastin expression in vitro and in vivo in the aorta of young adult rats. Therefore, we have studied the effect of a 10-week chronic oral treatment with Minoxidil (120 mg/L in drinking water) on the aortic structure and function in aged 24-month-old mice. Minoxidil treatment increased tropoelastin, fibulin-5, and lysyl-oxidase messenger RNA levels, reinduced a moderate expression of elastin, and lowered the levels of AGE-related molecules. This was accompanied by the formation of newly synthesized elastic fibers, which had diverse orientations in the wall. A decrease in the glycation capacity of aortic elastin was also produced by Minoxidil treatment. The ascending aorta also underwent a Minoxidil-induced increase in diameter and decrease in wall thickness, which partly reversed the age-associated thickening and returned the wall thickness value and strain-stress relation closer to those of younger adult animals. In conclusion, our results suggest that Minoxidil presents an interesting potential for arterial remodeling in an antiaging perspective, even when treating already aged animals.

Minoxidil is a potential neuroprotective drug for paclitaxel-induced peripheral neuropathy.[Pubmed:28349969]

Sci Rep. 2017 Mar 28;7:45366.

Chemotherapy-induced peripheral neuropathy (CIPN) is a common side effect of cancer treatment. No medication has been shown to be effective in the treatment of CIPN. This study aims to integrate the image-based high-content screening, mouse behavior models and mechanistic cell-based assays to discover potential neuroprotective drugs. Among screened compounds, Minoxidil showed the most potent neuroprotective effect against paclitaxel, with regard to neurite outgrowth of dorsal root ganglia (DRG). Minoxidil protected mice from thermal insensitivity and alleviated mechanical allodynia in paclitaxel-treated mice. The ultrastructure and quantified G-ratio of myelin integrity of sciatic nerve tissues supported the observations in mouse behavioral tests. The mechanistic study on DRG neurons suggested that Minoxidil suppressed neuroinflammation and remodeled the dysregulation of intracellular calcium homeostasis provoked by paclitaxel. Importantly, Minoxidil showed a synergistic anti-tumor effect with paclitaxel both in tumor xenograft models of cervical and breast cancer. Interestingly, the quantitative assays on hair length and hair growth both exhibited that Minoxidil significantly improved the hair quality after chemotherapy. Since Minoxidil is a drug approved by the Food and Drug Administration (FDA), the safety and biocompatibility are well documented. The immediate next step is to launch an early-stage clinical trial intending to prevent CIPN by Minoxidil.

Minoxidil dose response study in female pattern hair loss patients determined to be non-responders to 5% topical minoxidil.[Pubmed:28078868]

J Biol Regul Homeost Agents. 2016 Oct-Dec;30(4):1153-1155.

Topical Minoxidil is the only US FDA approved drug for the treatment of female pattern hair loss (FPHL). 5% Minoxidil foam is only effective at re-growing hair in a minority of women (approximately 40%). Thus, the majority of FPHL patients remain untreated. Previously, we demonstrated that nonresponders to 5% Minoxidil have low metabolism of Minoxidil in hair follicles. As such, we hypothesized that increasing the dosage of topical Minoxidil to low metabolizers would increase the number of responders without increasing the incidence of adverse events. In this study, we recruited FPHL subjects that were identified as non-responders to 5% topical Minoxidil utilizing the previously validated assay for Minoxidil response. Subjects were treated for 12 weeks with a novel 15% topical Minoxidil solution. At 12 weeks, 60% of subjects achieved a clinically significant response based on target area hair counts (>13.7% from baseline), as well as significant improvement in global photographic assessment. None of the subjects experienced significant hemodynamic changes or any other adverse events. To the best of our knowledge, this is the first study to demonstrate the potentially beneficial effect of a higher dosage of Minoxidil in FPHL subjects who fail to respond to 5% Minoxidil.

Minoxidil upregulates the expression of vascular endothelial growth factor in human hair dermal papilla cells.[Pubmed:9580790]

Br J Dermatol. 1998 Mar;138(3):407-11.

The hair follicle dermal papilla which controls hair growth, is characterized in the anagen phase by a highly developed vascular network. We have demonstrated in a previous study that the expression of an angiogenic growth factor called vascular endothelial growth factor (VEGF) mRNA varied during the hair cycle. VEGF mRNA is strongly expressed in dermal papilla cells (DPC) in the anagen phase, but during the catagen and telogen phases. VEGF mRNA is less strongly expressed. This involvement of VEGF during the hair cycle allowed us to determine whether VEGF mRNA expression by DPC was regulated by Minoxidil. In addition, the effect of Minoxidil on VEGF protein synthesis in both cell extracts and DPC-conditioned medium, was investigated immunoenzymatically. Both VEGF mRNA and protein were significantly elevated in treated DPC compared with controls. DPC incubated with increasing Minoxidil concentrations (0.2, 2, 6, 12 and 24 mumol/L) induced a dose-dependent expression of VEGF mRNA. Quantification of transcripts showed that DPC stimulated with 24 mumol/L Minoxidil express six times more VEGF mRNA than controls. Similarly, VEGF protein production increases in cell extracts and conditioned media following Minoxidil stimulation. These studies strongly support the likely involvement of Minoxidil in the development of dermal papilla vascularization via a stimulation of VEGF expression, and support the hypothesis that Minoxidil has a physiological role in maintaining a good vascularization of hair follicles in androgenetic alopecia.

Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats.[Pubmed:8133016]

J Hypertens. 1993 Dec;11(12):1337-45.

OBJECTIVE AND DESIGN: In spontaneously hypertensive rats (SHR) arterial vasodilators do not cause regression and might cause further progression of cardiac hypertrophy. To assess whether these effects extend to the vasculature, and to examine the possible mechanisms involved, cardiac and mesenteric arterial structure was evaluated with respect to changes in cardiac volume load and cardiac and arterial sympathetic activity during long-term (5- and 10-week) treatment of 16-week-old SHR with the arterial vasodilator Minoxidil, alone or in combination with the diuretic hydrochlorothiazide. RESULTS: Despite causing a persistent decrease in blood pressure in SHR, Minoxidil further increased left and right ventricular weights and left ventricular internal diameter. In combination with hydrochlorothiazide, Minoxidil caused concentric, rather than eccentric, left ventricular hypertrophy. In the mesenteric arterial bed of SHR, Minoxidil increased the lumen of the superior mesenteric artery, and prevented further increases in the medial area of the large and small mesenteric arteries. The increase in lumen size of the superior mesenteric artery by Minoxidil was abolished when hydrochlorothiazide was added to the treatment. After 10 weeks' treatment with Minoxidil, noradrenaline turnover rates were still significantly increased in the left ventricle but were decreased in the mesenteric arteries in the SHR. Minoxidil increased plasma and blood volumes, the increases being largely prevented by concomitant diuretic treatment. CONCLUSIONS: We conclude that there are regional differences in the response of the cardiovascular system to Minoxidil in SHR. Some of these differences may be related to differences in regional sympathetic activity, whereas volume load appears to play a modulatory role.

Minoxidil (U10858) is an ATP-sensitive potassium (KATP) channel opener, a potent oral antihypertensive agent and a peripheral vasodilator that promotes vasodilation also affects hair growth. Minoxidil is also a potent inhibitor of soybean lipoxygenaseare with an IC50 of 20 μM.

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