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Why antagonism of angiotensin II is unlogical on heavy compounds,by Mandy
Welcome back to another thread of Mandy,I constantly see people recommend telmisartan on steroid cycles,especially heavy ones.
Before clarifying,I am NOT telling to get rid of such a angiotensin II antagonist: I am merely just saying that expecting a angiotensin II antagonist is going to mitigate most side effects especially on heavy cycles is not a way.
heavy steroid cycles often engage multiple pathways affecting blood pressure and metabolism simultaneously, which single mechanism drugs rarely fully control.
1. What is a angiotensin II and what does an antagonist do?
Angiotensin II is a peptide endocrine hormone that plays an important factor in the renin-angiotensin-aldosterone system. It’s an inter related endocrine hormone system that is responsible for cardiovascular maintenance. Angiotensinogen which an alpha-globulin produced primarily by the liver, after synthesis it’s a vasopressin which acts on endothelial cells by the AT 1 and AT 2 receptor. Their signaling leads to calcium dependent phosphorylation of myosin,which impacts vascular smooth muscle contraction and would also lead to the main factor which is an increase blood pressure.
Now angiotensin II antagonists like telmisartan,don’t necessarily inhibit the production of angiotensinogen but just antagonizes binding at the AT 1 receptor.
Blocking AT1 receptors may reduce water retention and renal mediated blood pressure increases, but it doesn’t influence central adrenergic tone directly.
2. Why it’s almost irrelevant in heavy cycles especially with tren
Androgenic compounds during steroid cycles is almost guaranteed to increase your blood pressure especially at higher dosages or paired with most compounds,this is water. It does this by upregulating 20-HETE,which would activate NF-KB which increases oxidative stress and blood pressure. Since this is a renal factor,a angiotensin II antagonist such as telmisartan can do the job.
But no one counts in the fact that compounds such as tren can increase adrenegic tone by potent CNS stimulation,an increased adrenegic tone would raise blood pressure in another way and that is via the ẞ1 receptor. You can still take telmisartan and your blood pressure could be high,simply because ẞ1 is still being unregulated.
CNS-mediated β1 activation affects heart rate and contractility directly, bypassing the renal-angiotensin pathway, which is why telmisartan alone cannot fully normalize BP.
Mandy,what can you do against ß1 upregulation? This is an obvious answer,you can use a beta blocker that’s either selective on ẞ1 receptor such as bisoprolol or a non selective beta blocker that targets both ẞ1 and ẞ2 such as propanol. Reminder,ẞ2 is not responsible for the cardiovascular symptoms.
3. Other factors that it simply can’t overpower
Now many people on this forum such as Biomaxx promote telmisartan for issues against for example insulin sensitivity. Now if you were natty and not running GH,there would be an improvement of insulin sensitivity and blood glucose management.
But remember,if you’re going to run something like GH,no telmisartan would counteract the effect of hyperglycemia such as insulin simply because it would be trying to put down a house fire with a water gun.
GH raises blood glucose mainly via hepatic gluconeogenesis and peripheral insulin resistance pathways independent of RAAS modulation.
Thank you all for reading,I hope you all learned something out of this. If you notice a mistake I made,please point it out and explain me why.
Have a good day/night baby,Mandy will be back soon
Why antagonism of angiotensin II is unlogical on heavy compounds,by Mandy
Welcome back to another thread of Mandy,I constantly see people recommend telmisartan on steroid cycles,especially heavy ones.
Before clarifying,I am NOT telling to get rid of such a angiotensin II antagonist: I am merely just saying that expecting a angiotensin II antagonist is going to mitigate most side effects especially on heavy cycles is not a way.
heavy steroid cycles often engage multiple pathways affecting blood pressure and metabolism simultaneously, which single mechanism drugs rarely fully control.
1. What is a angiotensin II and what does an antagonist do?
Angiotensin II is a peptide endocrine hormone that plays an important factor in the renin-angiotensin-aldosterone system. It’s an inter related endocrine hormone system that is responsible for cardiovascular maintenance. Angiotensinogen which an alpha-globulin produced primarily by the liver, after synthesis it’s a vasopressin which acts on endothelial cells by the AT 1 and AT 2 receptor. Their signaling leads to calcium dependent phosphorylation of myosin,which impacts vascular smooth muscle contraction and would also lead to the main factor which is an increase blood pressure.
Now angiotensin II antagonists like telmisartan,don’t necessarily inhibit the production of angiotensinogen but just antagonizes binding at the AT 1 receptor.
Blocking AT1 receptors may reduce water retention and renal mediated blood pressure increases, but it doesn’t influence central adrenergic tone directly.
2. Why it’s almost irrelevant in heavy cycles especially with tren
Androgenic compounds during steroid cycles is almost guaranteed to increase your blood pressure especially at higher dosages or paired with most compounds,this is water. It does this by upregulating 20-HETE,which would activate NF-KB which increases oxidative stress and blood pressure. Since this is a renal factor,a angiotensin II antagonist such as telmisartan can do the job.
But no one counts in the fact that compounds such as tren can increase adrenegic tone by potent CNS stimulation,an increased adrenegic tone would raise blood pressure in another way and that is via the ẞ1 receptor. You can still take telmisartan and your blood pressure could be high,simply because ẞ1 is still being unregulated.
CNS-mediated β1 activation affects heart rate and contractility directly, bypassing the renal-angiotensin pathway, which is why telmisartan alone cannot fully normalize BP.
Mandy,what can you do against ß1 upregulation? This is an obvious answer,you can use a beta blocker that’s either selective on ẞ1 receptor such as bisoprolol or a non selective beta blocker that targets both ẞ1 and ẞ2 such as propanol. Reminder,ẞ2 is not responsible for the cardiovascular symptoms.
3. Other factors that it simply can’t overpower
Now many people on this forum such as Biomaxx promote telmisartan for issues against for example insulin sensitivity. Now if you were natty and not running GH,there would be an improvement of insulin sensitivity and blood glucose management.
But remember,if you’re going to run something like GH,no telmisartan would counteract the effect of hyperglycemia such as insulin simply because it would be trying to put down a house fire with a water gun.
GH raises blood glucose mainly via hepatic gluconeogenesis and peripheral insulin resistance pathways independent of RAAS modulation.
Thank you all for reading,I hope you all learned something out of this. If you notice a mistake I made,please point it out and explain me why.
Have a good day/night baby,Mandy will be back soon
Why antagonism of angiotensin II is unlogical on heavy compounds,by Mandy
Welcome back to another thread of Mandy,I constantly see people recommend telmisartan on steroid cycles,especially heavy ones.
Before clarifying,I am NOT telling to get rid of such a angiotensin II antagonist: I am merely just saying that expecting a angiotensin II antagonist is going to mitigate most side effects especially on heavy cycles is not a way.
heavy steroid cycles often engage multiple pathways affecting blood pressure and metabolism simultaneously, which single mechanism drugs rarely fully control.
1. What is a angiotensin II and what does an antagonist do?
Angiotensin II is a peptide endocrine hormone that plays an important factor in the renin-angiotensin-aldosterone system. It’s an inter related endocrine hormone system that is responsible for cardiovascular maintenance. Angiotensinogen which an alpha-globulin produced primarily by the liver, after synthesis it’s a vasopressin which acts on endothelial cells by the AT 1 and AT 2 receptor. Their signaling leads to calcium dependent phosphorylation of myosin,which impacts vascular smooth muscle contraction and would also lead to the main factor which is an increase blood pressure.
Now angiotensin II antagonists like telmisartan,don’t necessarily inhibit the production of angiotensinogen but just antagonizes binding at the AT 1 receptor.
Blocking AT1 receptors may reduce water retention and renal mediated blood pressure increases, but it doesn’t influence central adrenergic tone directly.
2. Why it’s almost irrelevant in heavy cycles especially with tren
Androgenic compounds during steroid cycles is almost guaranteed to increase your blood pressure especially at higher dosages or paired with most compounds,this is water. It does this by upregulating 20-HETE,which would activate NF-KB which increases oxidative stress and blood pressure. Since this is a renal factor,a angiotensin II antagonist such as telmisartan can do the job.
But no one counts in the fact that compounds such as tren can increase adrenegic tone by potent CNS stimulation,an increased adrenegic tone would raise blood pressure in another way and that is via the ẞ1 receptor. You can still take telmisartan and your blood pressure could be high,simply because ẞ1 is still being unregulated.
CNS-mediated β1 activation affects heart rate and contractility directly, bypassing the renal-angiotensin pathway, which is why telmisartan alone cannot fully normalize BP.
Mandy,what can you do against ß1 upregulation? This is an obvious answer,you can use a beta blocker that’s either selective on ẞ1 receptor such as bisoprolol or a non selective beta blocker that targets both ẞ1 and ẞ2 such as propanol. Reminder,ẞ2 is not responsible for the cardiovascular symptoms.
3. Other factors that it simply can’t overpower
Now many people on this forum such as Biomaxx promote telmisartan for issues against for example insulin sensitivity. Now if you were natty and not running GH,there would be an improvement of insulin sensitivity and blood glucose management.
But remember,if you’re going to run something like GH,no telmisartan would counteract the effect of hyperglycemia such as insulin simply because it would be trying to put down a house fire with a water gun.
GH raises blood glucose mainly via hepatic gluconeogenesis and peripheral insulin resistance pathways independent of RAAS modulation.
Thank you all for reading,I hope you all learned something out of this. If you notice a mistake I made,please point it out and explain me why.
Have a good day/night baby,Mandy will be back soon
valsartan does indeed mog but idk the mechanisms behind tbh
idk why nebivolol is promoted over eplerenone for gh bloat either
dont know the role of pde5 inhibition either tbh
Why antagonism of angiotensin II is unlogical on heavy compounds,by Mandy
Welcome back to another thread of Mandy,I constantly see people recommend telmisartan on steroid cycles,especially heavy ones.
Before clarifying,I am NOT telling to get rid of such a angiotensin II antagonist: I am merely just saying that expecting a angiotensin II antagonist is going to mitigate most side effects especially on heavy cycles is not a way.
heavy steroid cycles often engage multiple pathways affecting blood pressure and metabolism simultaneously, which single mechanism drugs rarely fully control.
1. What is a angiotensin II and what does an antagonist do?
Angiotensin II is a peptide endocrine hormone that plays an important factor in the renin-angiotensin-aldosterone system. It’s an inter related endocrine hormone system that is responsible for cardiovascular maintenance. Angiotensinogen which an alpha-globulin produced primarily by the liver, after synthesis it’s a vasopressin which acts on endothelial cells by the AT 1 and AT 2 receptor. Their signaling leads to calcium dependent phosphorylation of myosin,which impacts vascular smooth muscle contraction and would also lead to the main factor which is an increase blood pressure.
Now angiotensin II antagonists like telmisartan,don’t necessarily inhibit the production of angiotensinogen but just antagonizes binding at the AT 1 receptor.
Blocking AT1 receptors may reduce water retention and renal mediated blood pressure increases, but it doesn’t influence central adrenergic tone directly.
2. Why it’s almost irrelevant in heavy cycles especially with tren
Androgenic compounds during steroid cycles is almost guaranteed to increase your blood pressure especially at higher dosages or paired with most compounds,this is water. It does this by upregulating 20-HETE,which would activate NF-KB which increases oxidative stress and blood pressure. Since this is a renal factor,a angiotensin II antagonist such as telmisartan can do the job.
But no one counts in the fact that compounds such as tren can increase adrenegic tone by potent CNS stimulation,an increased adrenegic tone would raise blood pressure in another way and that is via the ẞ1 receptor. You can still take telmisartan and your blood pressure could be high,simply because ẞ1 is still being unregulated.
CNS-mediated β1 activation affects heart rate and contractility directly, bypassing the renal-angiotensin pathway, which is why telmisartan alone cannot fully normalize BP.
Mandy,what can you do against ß1 upregulation? This is an obvious answer,you can use a beta blocker that’s either selective on ẞ1 receptor such as bisoprolol or a non selective beta blocker that targets both ẞ1 and ẞ2 such as propanol. Reminder,ẞ2 is not responsible for the cardiovascular symptoms.
3. Other factors that it simply can’t overpower
Now many people on this forum such as Biomaxx promote telmisartan for issues against for example insulin sensitivity. Now if you were natty and not running GH,there would be an improvement of insulin sensitivity and blood glucose management.
But remember,if you’re going to run something like GH,no telmisartan would counteract the effect of hyperglycemia such as insulin simply because it would be trying to put down a house fire with a water gun.
GH raises blood glucose mainly via hepatic gluconeogenesis and peripheral insulin resistance pathways independent of RAAS modulation.
Thank you all for reading,I hope you all learned something out of this. If you notice a mistake I made,please point it out and explain me why.
Have a good day/night baby,Mandy will be back soon
Why antagonism of angiotensin II is unlogical on heavy compounds,by Mandy
Welcome back to another thread of Mandy,I constantly see people recommend telmisartan on steroid cycles,especially heavy ones.
Before clarifying,I am NOT telling to get rid of such a angiotensin II antagonist: I am merely just saying that expecting a angiotensin II antagonist is going to mitigate most side effects especially on heavy cycles is not a way.
heavy steroid cycles often engage multiple pathways affecting blood pressure and metabolism simultaneously, which single mechanism drugs rarely fully control.
1. What is a angiotensin II and what does an antagonist do?
Angiotensin II is a peptide endocrine hormone that plays an important factor in the renin-angiotensin-aldosterone system. It’s an inter related endocrine hormone system that is responsible for cardiovascular maintenance. Angiotensinogen which an alpha-globulin produced primarily by the liver, after synthesis it’s a vasopressin which acts on endothelial cells by the AT 1 and AT 2 receptor. Their signaling leads to calcium dependent phosphorylation of myosin,which impacts vascular smooth muscle contraction and would also lead to the main factor which is an increase blood pressure.
Now angiotensin II antagonists like telmisartan,don’t necessarily inhibit the production of angiotensinogen but just antagonizes binding at the AT 1 receptor.
Blocking AT1 receptors may reduce water retention and renal mediated blood pressure increases, but it doesn’t influence central adrenergic tone directly.
2. Why it’s almost irrelevant in heavy cycles especially with tren
Androgenic compounds during steroid cycles is almost guaranteed to increase your blood pressure especially at higher dosages or paired with most compounds,this is water. It does this by upregulating 20-HETE,which would activate NF-KB which increases oxidative stress and blood pressure. Since this is a renal factor,a angiotensin II antagonist such as telmisartan can do the job.
But no one counts in the fact that compounds such as tren can increase adrenegic tone by potent CNS stimulation,an increased adrenegic tone would raise blood pressure in another way and that is via the ẞ1 receptor. You can still take telmisartan and your blood pressure could be high,simply because ẞ1 is still being unregulated.
CNS-mediated β1 activation affects heart rate and contractility directly, bypassing the renal-angiotensin pathway, which is why telmisartan alone cannot fully normalize BP.
Mandy,what can you do against ß1 upregulation? This is an obvious answer,you can use a beta blocker that’s either selective on ẞ1 receptor such as bisoprolol or a non selective beta blocker that targets both ẞ1 and ẞ2 such as propanol. Reminder,ẞ2 is not responsible for the cardiovascular symptoms.
3. Other factors that it simply can’t overpower
Now many people on this forum such as Biomaxx promote telmisartan for issues against for example insulin sensitivity. Now if you were natty and not running GH,there would be an improvement of insulin sensitivity and blood glucose management.
But remember,if you’re going to run something like GH,no telmisartan would counteract the effect of hyperglycemia such as insulin simply because it would be trying to put down a house fire with a water gun.
GH raises blood glucose mainly via hepatic gluconeogenesis and peripheral insulin resistance pathways independent of RAAS modulation.
Thank you all for reading,I hope you all learned something out of this. If you notice a mistake I made,please point it out and explain me why.
Have a good day/night baby,Mandy will be back soon
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Biomaxx promote telmisartan for issues against for example insulin sensitivity. Now if you were natty and not running GH,there would be an improvement of insulin sensitivity and blood glucose management.
