aas-222Bodybuilders abuse androgens that make kidneys to release EPO.
As a result hemopoiesis will elevate hemoglobin and hematoctrite.
Thus, bloods viscosity increases and blood becomes thicker.
This is a serious factor for ischemic stroke, because can lead to occlusion of cerebral arteries.
This occurs even more easily, especially if athlete smokes.
Nicotine is known to promote platelets aggregation.

Moreover, bodybuilders abuse CNS stimulants in order to enhance beta oxidation of adipose tissue. Ephedrine & Clenbuterol HCL, thyroxine and triodothyronine, amphetamines and caffeine are among them.
These adrenergic sympatheticomimetic substances, elevate systemic blood pressure (BP) dramatically, both systolic and diastolic.
As a result, a cerebral aneurism is highly likely to occur, under stressing circumstances, such as squats or HIIT.
Ischemic strokes have usually better prognosis, rather than hemorrhagic strokes.
In hemorrhagic stroke, the area where blood is spread into cerebral cortex, is destroyed and equals with cellular death.
Hemorrhage compresses cortex and edema takes place.

Another factor that elevates BP is aldosterone hormone.
As we know, AAS promote water retention, known as edema into the muscle.
This is the result of sodium retention, the main extracellular element.
AAS that aromatise, lead to water retention as well.
Estrogens are linked with this edema and puffy look.
Therefore a bodybuilder under off season, who abuses steroids that aromatise, has greater chances of developing hypertension.

However, few AAS that don’t aromatise are capable to increase BP (Patrick Arnold)
Flyoxymesterone and trenbolone are among them.
Both of them suppress the catabolic glucocorticosteroid  cortisol (this is the reason of their high anabolic effect).
But they also suppress the mineralcorticosteroid aldosterone.
So this is the reason they have zero water retention (Peter Van Mol).

However, other mechanisms that involve inhibition of the enzyme 11 hydroxylase, will eventually lead to increased BP.
Kidneys have this specific enzyme, in order to protect them from BP that occurs from cortisol.
This enzyme converts cortisol into the inactive cortisone (synthetic form).
The reason of that is the fact aldosterone’s receptors are sometimes bound by cortisol and the problem initiates.
When inhibition of 11 hydroxylase occurs, another corticosteroid deoxycorticosterone is synthesized, leading to increased BP (Nelson Vergel)

AAS induce thromboembolism, through another mechanism.
Fibrinogen is a clotting factor elevated under steroid abuse.
Thus, blood is more likely to form clots and embolism.
Tobacco also promotes thrombosis, through nicotine. This substance is known to disrupt the endothelium of arteries, leading to platelets aggregation.
As preventing rules, the use of salicylic acid will inhibit platelets agreggation.
A diet low in sodium also helps, while blood donation lowers bloods volume.

AAS-INDUCED HYPERTENSION

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