RENIN-ANGIOTENSIN-ALDOSTERONE SYSYTEM And HAIR LOSS PROCESS

[johnwester130]

@md_a

is perindopril comparable to spironolactone/eplerenone?

 

[ReSTART]

balding is caused by fibrosis, calcification and inflammation of tissue around hair follicle and of the scalp

dotor just want minox, finasteride and maybe ketoconazole

minox (pge2 and nitric oxide releaser) and finasteride (dht blocker) both toxic

fibrosis calcification inflammation

voltage-gated calcium-channels in cells
potassium, sodium (salt)
calcium, potassium

spironolactone decreases potassium excretion, while blocking reabsorption of chloride and sodium ions, lowering blood pressure.

clonidine increases arr (aldosterone to renin ratio) and spironolactone decreases it, i dont know what effect has

 

[md_a]

@md_a

is perindopril comparable to spironolactone/eplerenone?

Impact of atrovastatin and perindopril on the hair cycle in rodent model – risk of drug induced alopecia in patients with heart disease

Perindopril belongs to ACE inhibitors and drug-induced hair loss occurs in 1-5% of treated patients. According to available data, it is observed both in adults and children.

Based on the course of the spontaneous and induced hair cycles the relationship between telogen effluvium and perindopril intake was proven. The hair loss evolved slowly during the experiment. There were only slight differences between tested and control groups during the first spontaneous and induced hair cycles. It was due to premature hair follicle involution not followed by the telogen synchronization. II and III induced and spontaneous hair cycles showed progression of the hair follicle destruction. The premature hair follicle involution was followed by the telogen synchronization and showed toxic effect of the drug responsible for the alopecia. Analysis of the induced and spontaneous hair cycles in time confirmed time related hair follicle destruction, leading to the chronic drug-induced alopecia

ACE inhibitors on zinc levels was also studied (19). During 9 weeks of experiment animals received 2 mg of captopril intraperitoneally. Afterwards zinc levels were determined in indicated tissues. The hair zinc concentration was significantly decreased. It confirmed the role of perindopril in zinc metabolism and in alopecia occurrence. Especially due to fact that, hair loss in rats is related to zinc deficiency (9).

CONCLUSIONS
Perindopril has also toxic effect on the hair follicle and is responsible for drug-induced alopecia. Observed telogen effluvium is chronic and associated with prolonged therapy. In rats clinical outcome is late and involve hair shedding on the lateral body sides.

 

[johnwester130]

Impact of atrovastatin and perindopril on the hair cycle in rodent model – risk of drug induced alopecia in patients with heart disease

Perindopril belongs to ACE inhibitors and drug-induced hair loss occurs in 1-5% of treated patients. According to available data, it is observed both in adults and children.

Based on the course of the spontaneous and induced hair cycles the relationship between telogen effluvium and perindopril intake was proven. The hair loss evolved slowly during the experiment. There were only slight differences between tested and control groups during the first spontaneous and induced hair cycles. It was due to premature hair follicle involution not followed by the telogen synchronization. II and III induced and spontaneous hair cycles showed progression of the hair follicle destruction. The premature hair follicle involution was followed by the telogen synchronization and showed toxic effect of the drug responsible for the alopecia. Analysis of the induced and spontaneous hair cycles in time confirmed time related hair follicle destruction, leading to the chronic drug-induced alopecia

ACE inhibitors on zinc levels was also studied (19). During 9 weeks of experiment animals received 2 mg of captopril intraperitoneally. Afterwards zinc levels were determined in indicated tissues. The hair zinc concentration was significantly decreased. It confirmed the role of perindopril in zinc metabolism and in alopecia occurrence. Especially due to fact that, hair loss in rats is related to zinc deficiency (9).

CONCLUSIONS
Perindopril has also toxic effect on the hair follicle and is responsible for drug-induced alopecia. Observed telogen effluvium is chronic and associated with prolonged therapy. In rats clinical outcome is late and involve hair shedding on the lateral body sides.

Thank you


great find

 

[md_a]

Thank you


great find

From what I've read, I think that blocking AT1R could help regenerate hair, and I think that a gel-like valsartan gel, applied topically could have an effect, but I'm just speculating. So, everything that inhibits this AT1 receptor has a total beneficial effect on the body and combined with acetazolamide, for example, I think it is a good solution, and it is worth testing.

……..

The topical application of 1% AT1R inhibition valsartan gel, compared with other tested formulations or placebo, facilitated and significantly accelerated closure time and increased tensile strength in mice, and was validated in the porcine model [35]. The RAS is known to be dysregulated in diabetes, with increased AT1R and decreased AT2R expression in diabetic wound healing, which may play a role in the skin vulnerability associated with diabetes [[36], [37], [38]]. Diabetic patients exposed to ACE inhibitors are more likely to develop foot ulcers than those exposed to ARB, indicating a potential role of AT2R-mediated protection in a diabetic setting [39]. at the same time, topical application of captopril has also already been shown to delay healing of wounds in diabetic mice [35]. Because diabetes could induce the dysfunction of several stem cells including ECSs [[40], [41], [42]], it is intriguing whether AT2R activation in ESCs enhances its function, thereby facilitating healing of diabetic refractory skin wounds.

Critical role of the endogenous renin-angiotensin system in maintaining self-renewal and regeneration potential of epidermal stem cells

…………

We investigated the effect of angiotensin II (Ang II) on matrix metalloproteinase-1 (MMP-1)/tissue inhibitor of metalloproteinase-1 (TIMP-1) balance in regulating collagen metabolism of diabetic skin. Skin tissues from diabetic model were collected, and the primary cultured fibroblasts were treated with Ang II receptor inhibitors before Ang II treatment. The collagen type I (Coll I) and collagen type III (Coll III) were measured by histochemistry. The expressions of transforming growth factor-β (TGF-β), MMP-1, TIMP-1 and propeptides of types I and III procollagens in skin tissues and fibroblasts were quantified using polymerase chain reaction (PCR), Western blot or enzyme-linked immunosorbent assay (ELISA). Collagen dysfunction was documented by changed collagen I/III ratio in streptozotocin (STZ)-injected mice compared with controls. This was accompanied by increased expression of TGF-β, TIMP-1 and propeptides of types I and III procollagens in diabetic skin tissues. In primary cultured fibroblasts, Ang II prompted collagen synthesis accompanied by increases in the expressions of TGF-β, TIMP-1 and types I and III procollagens, and these increases were inhibited by losartan, an Ang II type 1 (AT1) receptor blocker, but not affected by PD123319, an Ang II type 2 (AT2) receptor antagonist. These findings present evidence that Ang-II-mediated changes in the productions of MMP-1 and TIMP-1 occur via AT1 receptors and a TGF-β-dependent mechanism.

Angiotensin II regulates collagen metabolism through modulating tissue inhibitor of metalloproteinase-1 in diabetic skin tissues - PubMed

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Results: Our experiments demonstrated the localization of AT1 in the inner root sheath and the inner layers of the outer root sheath. In BCC, positive staining with AT1 was revealed in the tumour cells of basal cell carcinoma with follicular differentiation.



Conclusions: AT1 may have a role in association with follicular keratinization. Studying AT1 distribution may be useful in understanding the pathophysiology of human hair follicles and the hair follicle-associated tumours.

Immunohistochemical study of angiotensin receptors in human anagen hair follicles and basal cell carcinoma - PubMed

………..


Angiotensin II receptor blockade promotes repair of skeletal muscle through down-regulation of aging-promoting C1q expression

Disruption of angiotensin II type 1 (AT1) receptor prolonged life span in mice. Since aging-related decline in skeletal muscle function was retarded in Atgr1a−/− mice, we examined the role of AT1 receptor in muscle regeneration after injury. Administration of AT1 receptor blocker irbesartan increased the size of regenerating myofibers, decreased fibrosis and enhanced functional muscle recovery after cryoinjury. We recently reported that complement C1q, secreted by macrophages, activated Wnt/β-catenin signaling and promoted aging-related decline in regenerative capacity of skeletal muscle. Notably, irbesartan induced M2 polarization of macrophages, but reduced C1q expression in cryoinjured muscles and in cultured macrophage cells. Irbesartan inhibited up-regulation of Axin2, a downstream gene of Wnt/β-catenin pathway, in cryoinjured muscles. In addition, topical administration of C1q reversed beneficial effects of irbesartan on skeletal muscle regeneration after injury. These results suggest that AT1 receptor blockade improves muscle repair and regeneration through down-regulation of the aging-promoting C1q-Wnt/β-catenin signaling pathway.

Angiotensin II receptor blockade promotes repair of skeletal muscle through down-regulation of aging-promoting C1q expression - Scientific Reports

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[ReSTART]

beta-blockers, clonidine and nsiads increases arr (aldosterone to renin ratio) by decreasing aldosterone concentration less than renin.

salt restriction, angiotensin enzyme blockers, diuretics (like spironolactone), dihydropyridine calcium channel blockers (CCBs), and angiotensin II receptor blockers (ARBs) reduce ARR, by decreasing renin less than aldosterone.

 

[ReSTART]

angiotensin is made from angiotensinogen in the liver using renin, into angiotensin I then into angiotensin II. angiotensin I seems to have minimal biological action.

angiotensin I is converted into II by the ACE enzyme that the ACE inhibitors block.

angiotensin II increases aldosterone secretion and vasopressin production.

angiotensin II increases sodium retention and potassium excretion.

 

[golder]

Wow, pages and pages of incredibly dense information here, thanks to all who have shared. I’m going to be a hypocrite and ask the question I normally cringe at when I see, but can anyone help condense some of the most compelling findings from this thread. I’m going to eventually read it in its entirety, but I’m trying to custom make a hair loss stack now and I wanted to know if there’s any promising findings from here that might make worthy additions to the protocol? Thanks in advance!

 

[Candeias]

I didn't read the whole topic but I'm wondering are -sartans useful for hair loss?