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The.Shadow
02-14-2018, 11:54 AM
Cardiac hypertrophy is a very real side effect of PED use that all users should actively be working to minimise over time, and inhibiting activation of the RAAS is something that could be considered to help with this goal in respect to AAS use.

RAAS = renin–angiotensin–aldosterone system. RAAS regulates arterial blood pressure, water and electrolyte balance, but pathological activation results in vasoconstriction, vascular and cardiac hypertrophy and fibrosis.

It appears all AAS activate RAAS, but some animal studies seem to point toward varying degrees, with nandrolone seemingly being the worst culprit. (although, I have never seen human data on this).

Blocking RAAS has shown benefit for hypertension, heart attack, chronic heart failure, stroke and renal disease.

ACE Inhibitors and angiotensin are both clinically effective for inhibiting RAAS activation. ARB's seem to be the most commonly prescribed medication as ACEI's do cause intollerance issues in many.

Renin–angiotensin–aldosterone system blockade for cardiovascular diseases: current status (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938800/)
AT1 and aldosterone receptors blockade prevents the chronic effect of nandrolone on the exercise-induced cardioprotection in perfused rat heart sub... - PubMed - NCBI (https://www.ncbi.nlm.nih.gov/pubmed/24258356)
Renin-angiotensin-aldosterone system in bodybuilders using supraphysiological doses of anabolic-androgenic steroids (PDF Download Available) (https://www.researchgate.net/publication/253242139_Renin-angiotensin-aldosterone_system_in_bodybuilders_using_supraphys iological_doses_of_anabolic-androgenic_steroids)


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