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jody

gh water retention

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at 4IU/day i see results but get a puffy bloated face and hands. anything to help. not using any AS, using syntheselene, proviron and exemestane. cant think of anything else to help. any info?

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The water retention from HGH is due to increased secretion of ADH (anti-diuretic hormone) from the posterior pituitary. The water retention and hypertension are controlled by .2mg of clonidine q 12 hours. Clonidine's primary action is retarding ADH secretion.

 

 

 

 

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The water retention from HGH is due to increased secretion of ADH (anti-diuretic hormone) from the posterior pituitary. The water retention and hypertension are controlled by .2mg of clonidine q 12 hours. Clonidine's primary action is retarding ADH secretion.

 

 

Is the mechanism behind AAS-induced hypertension similar, increased expression of vasopressin?

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Is the mechanism behind AAS-induced hypertension similar, increased expression of vasopressin?

 

No, AAS-induced hypertension is most often the result of water retention caused by aromatase and not a result of a raised secretion of vasopressin/ADH.

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No, AAS-induced hypertension is most often the result of water retention caused by aromatase and not a result of a raised secretion of vasopressin/ADH.

 

How does one explain it in non-aromatisable steroids then? I'm not being flip, I really am curious.

 

You have seen this sort of research?

 

Physiol Behav. 1996 Jul;60(1):25-9

Testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.

 

Psychiatry Department, University of Massachusetts Medical Center, Worcester 01655, USA.

 

In many species, testosterone treatment facilitates offensive aggression tested in resident-intruder models. As the mechanisms of action of testosterone remain unclear, we hypothesized that testosterone interacts with neurotransmitter systems involved in the regulation of offensive aggression. We tested this hypothesis with the vasopressinergic system in golden hamsters in three separate experiments. First, we compared the density of V1 vasopressin (VAP) receptor binding between castrated animals treated with testosterone and their untreated controls. The most noticeable difference was found within the ventrolateral hypothalamus (VLH), a site involved in the control of aggression in several species of mammals. Within this area, V1 AVP receptor binding disappeared after castration, while being maintained by testosterone-treatment. Second, we tested behavioral effects of AVP within the VLH. Microinjections of AVP (100 nl, 1 or 100 microM) within the VLH accelerated the onset of offensive aggression in testosterone-treated animals. However, AVP-injected animals did not bite more than their vehicle-injected controls. Third, microinjections of AVP failed to activate offensive aggression in animals deprived of testosterone. As AVP receptors appeared to overlay previously described distributions of androgen and estrogen receptors in golden hamsters, we propose that testosterone facilitates the onset of offensive aggression, at least partly, through an activation of AVP receptors within the VLH.

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I can only guess which other mechanisms are involved that cause hypertension by AAS.

 

Please do because it will assist in elucidating the best peventative treatment. If it is indeed vasopressin related then clonidine or demeclocycline would be the ideal choice or even HCTZ...if not, then some other treatment like an ace inhibitor or a calcium chanel blocker might be better...

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I would use 1/4-1/2 grain/day thyroid and use GH as long as possiable. I used for 10 months HGH at age 35 and I got 1 inch taller but I was using 10mg/day ( customs seizure papers said 10mg/vial) for a long time and I weened to 6iu/day at finish. From 6'00" before to 6'1" after.

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