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Blood pressure on cycle - causes and cures?

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redflash

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Here's a quick summary of what I know (or think I know) so that someone who knows more can share...

I believe there are two main causes of raised BP when on cycle.

The first is water retention caused by aromatisation of testosterone to estrogen. Best way to deal with this is to control (but not eliminate as it hasd good effects too) estrogen through either stopping the aromatisatio in the first place (Arimidex, Aromasin, Letro, etc) or blocking it at the receptor (Nolva/Tamoxifen, Clomid).

The second is increased red bloodcell count (RBC) which in layman's terms "thickens" the blood. Many AAS do this to some extent but Equipoise (EQ) seems to be the worst offender from what I read. Some folk recommend giving blood as the body quickly replaces the fluid. Low dose aspirin is used to "thin" the blood for those who have suffered a stroke or heart attack but I guess this doesn't work by reducing RBC so it may not help.

Am I missing anything? If I avoid, limit or control aromatising AAS (Test is my favourite so I control it), and steer clear of EQ, is that the best I can do?

Basically I am nearly 50 years old and though my BP is good when off-cycle and far from dangerous when on, I sometimes go a nice shade of beetroot which gives the game away...

Don't tell me to do more cardio, I have that covered!

Blackflash
 
Whats your bodyfat percentage and what cycles are you running??
 
10% and usually Test E and Anavar or Primo for the collagen synthesis.

Reason for question is that I am think of trying a different cycle, probably with Test E as a base but possibly with EQ instead of Primo/Anavar. Also thinking of where Proviron might play in (see separate thread).

I'm not looking for advice at this stage on which compounds to use, in what quantities and for how long; I'm just seeking to understand the mechanisms which increase BP (eg. do androgens have an effect which is nothing to do with RBC or aromatisation) and what can be done to address them.

I tried to make the question specific to minimise the number of people who respond by saying "all you need is nolva" or "letro is tops" which doesn't exactly increas my knowledge base...

All the best, and thanks in advance for any help.

Redflash
 
Last edited:
What dosages are you running?

Im asking in relation to your raised blood pressure concern!
 
Shadow,

I think you're trying to leap straight to a cure here and I may not even have a problem yet! Measured my off-cycle BP this morning at a healthy 120 over 78; on cycle it can rise into the 130's. That's far from dangerous.

I have run Test E at 500mg/week and last time at 700mg/week plus 60mg Anavar per day. I use Arim as my main anti-e.

I'm looking to understand the BP mechanisms, not go straight to possible cures, before I start tinkering with this base cycle. It would be helpful if you know whether the two BP mechanisms I have identified (water and RBC) are the only ones and we'll take it from there...

All the best,

Redflash
 
If you can lay off the orals, your bp will be better. Normally injectables don't affect bp as much.
 
^^ I'm very glad you brought this up, dg - oral contraceptives do this to women as well, although the patch and transdermal hormones do not.

This paragraph explains the process better than I ever could:


The Renin-Angiotensin-Aldosterone System
Previous studies using oral estrogens have demonstrated increases in PRA and aldosterone, likely through a hepatic-induced increase in angiotensinogen.19 20 Indeed, this activation of the RAAS has been proposed as a potential mechanism of estrogen-associated hypertension. Transdermal estrogen avoids this effect on the liver, and no effect on PRA or aldosterone has been shown in this and prior studies.21

In this study we measured both total and active renin and demonstrated that although estradiol increased total renin, it did not increase active renin. An increase in prorenin and total renin was seen without a concomitant increase in active renin or plasma renin activity. This finding supports the observational study by Schunkert et al,22 which showed that estrogen use is not associated with a rise of active renin. There are several possible explanations for this finding of the present study. It is possible that estradiol accelerates the metabolism of renin. However, this explanation would not account for the increase in total renin seen with estradiol administration. There is an estrogen response element on the promoter region of the angiotensinogen gene23 24 and a putative estrogen response element on the renin promoter as well.25 26 Thus, one would anticipate that estradiol would increase transcription of renin message, as reflected in the increase in total renin. As demonstrated by this study, however, it is likely that estradiol has another heretofore unknown effect on the RAAS: inhibition of the conversion of precursor renin into active renin. This inhibitory effect is supported in 4 ways: no change in active renin, PRA, and aldosterone levels and a rise in prorenin that parallels the rise in total renin. Angiotensinogen levels were not measured in this study. However, previous studies using transdermal patch estradiol did not report a change in angiotensinogen levels.21 22 Finally, this finding is unlikely to be secondary to some peculiarity of the RAAS in the population studied since the addition of progesterone produced a substantial activation of the RAAS. An inhibition of the activation of the RAAS by estradiol may play an important role in its ability to lower BP.

In conclusion, administration of transdermal estradiol with or without progesterone has a hypotensive effect, particularly at night, in postmenopausal women. Furthermore, estradiol appears to have a dual effect on renin: it increases its production but inhibits its activation. Further studies are required to affirm the first conclusion, using a clinical trial format, and to determine the mechanism(s) responsible for the second effect.​

Orals really suck, don't they?
 
dg806 said:
If you can lay off the orals, your bp will be better. Normally injectables don't affect bp as much.
Click to expand...

Now I'm really confused... or in denial... or just plain old disagreeing with you based on experience. I typically use Test E at around 500-700mg per week and Anavar at 40-60mg per day. That's it apart from auxiliaries like HCG and Arim.

Are you really saying that Anavar will raise my BP more than Test?

Are you really saying that my BP will be lower if I substitute (injectable) EQ for (oral) Anavar, despite EQ's reputation for increasing BP through increasing red blood cell count (RBC)? I'm pretty sure when I did try EQ my BP increased more than on Anavar!

Are you really saying that ALL orals increase BP more than ALL injectables? That's quite a generalisation...

I'm confused myself, and I think most people who've read the boards will also be confused. Can you explain why this should be the case?

I don't have a major BP issue right now but i'm thinking of trying a different cycle next time so being a good boy and doing my research. And it's not proving easy.

Thanks in advance,

Redflash
 
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redflash said:
Shadow,

I think you're trying to leap straight to a cure here and I may not even have a problem yet! Measured my off-cycle BP this morning at a healthy 120 over 78; on cycle it can rise into the 130's. That's far from dangerous.

I have run Test E at 500mg/week and last time at 700mg/week plus 60mg Anavar per day. I use Arim as my main anti-e.

I'm looking to understand the BP mechanisms, not go straight to possible cures, before I start tinkering with this base cycle. It would be helpful if you know whether the two BP mechanisms I have identified (water and RBC) are the only ones and we'll take it from there...

All the best,

Redflash
Click to expand...

dg806 said:
If you can lay off the orals, your bp will be better. Normally injectables don't affect bp as much.
Click to expand...

Built said:
^^ I'm very glad you brought this up, dg - oral contraceptives do this to women as well, although the patch and transdermal hormones do not.

This paragraph explains the process better than I ever could:


The Renin-Angiotensin-Aldosterone System
Previous studies using oral estrogens have demonstrated increases in PRA and aldosterone, likely through a hepatic-induced increase in angiotensinogen.19 20 Indeed, this activation of the RAAS has been proposed as a potential mechanism of estrogen-associated hypertension. Transdermal estrogen avoids this effect on the liver, and no effect on PRA or aldosterone has been shown in this and prior studies.21

In this study we measured both total and active renin and demonstrated that although estradiol increased total renin, it did not increase active renin. An increase in prorenin and total renin was seen without a concomitant increase in active renin or plasma renin activity. This finding supports the observational study by Schunkert et al,22 which showed that estrogen use is not associated with a rise of active renin. There are several possible explanations for this finding of the present study. It is possible that estradiol accelerates the metabolism of renin. However, this explanation would not account for the increase in total renin seen with estradiol administration. There is an estrogen response element on the promoter region of the angiotensinogen gene23 24 and a putative estrogen response element on the renin promoter as well.25 26 Thus, one would anticipate that estradiol would increase transcription of renin message, as reflected in the increase in total renin. As demonstrated by this study, however, it is likely that estradiol has another heretofore unknown effect on the RAAS: inhibition of the conversion of precursor renin into active renin. This inhibitory effect is supported in 4 ways: no change in active renin, PRA, and aldosterone levels and a rise in prorenin that parallels the rise in total renin. Angiotensinogen levels were not measured in this study. However, previous studies using transdermal patch estradiol did not report a change in angiotensinogen levels.21 22 Finally, this finding is unlikely to be secondary to some peculiarity of the RAAS in the population studied since the addition of progesterone produced a substantial activation of the RAAS. An inhibition of the activation of the RAAS by estradiol may play an important role in its ability to lower BP.

In conclusion, administration of transdermal estradiol with or without progesterone has a hypotensive effect, particularly at night, in postmenopausal women. Furthermore, estradiol appears to have a dual effect on renin: it increases its production but inhibits its activation. Further studies are required to affirm the first conclusion, using a clinical trial format, and to determine the mechanism(s) responsible for the second effect.​

Orals really suck, don't they?
Click to expand...

redflash said:
Now I'm really confused... or in denial... or just plain old disagreeing with you based on experience. I typically use Test E at around 500-700mg per week and Anavar at 40-60mg per day. That's it apart from auxiliaries like HCG and Arim.

Are you really saying that Anavar will raise my BP more than Test?

Are you really saying that my BP will be lower if I substitute (injectable) EQ for (oral) Anavar, despite EQ's reputation for increasing BP through increasing red blood cell count (RBC)? I'm pretty sure when I did try EQ my BP increased more than on Anavar!

Are you really saying that ALL orals increase BP more than ALL injectables? That's quite a generalisation...

I'm confused myself, and I think most people who've read the boards will also be confused. Can you explain why this should be the case?

I don't have a major BP issue right now but i'm thinking of trying a different cycle next time so being a good boy and doing my research. And it's not proving easy.

Thanks in advance,

Redflash
Click to expand...

Redflash, you asked a specific question: what factors beyond water-retention and erythropoiesis influence the increased blood pressure seen by many on a cycle?

dg806 answered that one - orals - which is supported in the literature, mediated by the activation of the RAAS.

In short, it's one more thing. If you don't want your blood pressure to go up on a cycle, don't go on.
 
Built said:
Redflash, you asked a specific question: what factors beyond water-retention and erythropoiesis influence the increased blood pressure seen by many on a cycle?

dg806 answered that one - orals - which is supported in the literature, mediated by the activation of the RAAS.

In short, it's one more thing. If you don't want your blood pressure to go up on a cycle, don't go on.
Click to expand...

Ok, Built, gotcha but... I'm a bright guy and I don't understand from anything here WHY or HOW orals (all orals) increase BP. If not water retention and not erythropoiesis then via what mechanism? Sorry if this is in your quoted article in scientific language I don't understand but I guess others won't understand it either.

Supplementary and very specific question then becomes this: based on that mechanism, will an all injectables cycle of 500mg Test E and 400mg EQ increase BP less than a cycle of 500mg Test E and 40mg Anavar (oral obviously) per day? If you and dg are saying "yes" then this has been a very valuable conversation indeed...
 
The point is, they all increase BP to a certain extent. The degree to which these individual components affect you, personally will depend upon many factors, including your health, age, existing health problems, diet, activity level, and of course the composition, dosing and duration of your cycle.

Oral estrogen / oral contraceptive, like oxandrolone and most other oral steriods, must be C-17 methylated in order to eliminate first-pass degradation in the liver. The methyl group is broken off by the liver, right? Without digging around more for clues, my guess would be that the action of doing so in the liver stimulates the release of aldosterone. The cited paragraph notes renin's involvement in this chain of events. Note the word "renin" has the same root as "renal".

Aldosterone is one of the hormones that governs sodium and water-retention, as well as potassium excretion.

When aldosterone is high, the body works to conserve sodium and water.

So the cascade would go ingestion of C-17 methylated steroid -> liver releases renin -> angiotensin increases -> aldosterone increases -> water and sodium are conserved, potassium is decreased -> blood pressure increases.

Or I'm on crack. Either/or.
 
They all raise BP levels, IMHO, orals raise them quicker.

My BP levels sky rocket when I'm peaking with dbol or anadrol in the gym, as well with tren. Taking a 1/2gr. shot of test e will not boost my PB right away....may have to wait 3-4 weeks.

/V
 
Built, let me check I hear you right. The fact that all orals and injectables increase BP "to a certain extent" is inarguable; what we're discussing here is the comparative extent to which most injectables and most orals do this in most people...

You're saying Anavar raises BP through increasing water retention, not because it aromatises (it doesn't) but because it's C17-alpha-alkylated. Firstly, I thought Anavar was used pre-contest partly because it does not cause water retention. Secondly, that would imply that Primobolan Acetate which is not C17-alpha-alkylated would not increase BP. Is that your hypothesis?

Victor, with respect (as they say) there is a world of difference between anavar and primo as orals and anadrol and dbol - the second two are much harder on the liver and they aromatise, givng a double-whammy effect on BP which they're well known for. What I'm trying to do here is test a hypothesis that ALL (or most) orals increase BP more than ALL (or most) injectables in ALL (or most) people i.e. the delivery mechanism (pills vs shots) is at least as important as the compound. That's potentially revolutionary...

Both: I'm pretty sure most people, before they read this thread, would expect a bigger hit on BP by a cycle of Test and Deca or Test and Tren (both injectables) than Test E shots and Primo tabs. I'm pretty sure that most people would not expect a significant difference in water retention and hence BP between Winstrol Depot and tabs or between Primo Depot and tabs.

If what Built and DG are saying is true then we're close to needing to tidy up this thread and make a sticky out of it to dispel a few myths, not just for anyone who wants to control their BP but for anyone who wants to control their water retention pre-contest etc.

RF
 
Anavar raises BP through RAAS-mediated upregulation of aldosterone, which changes the relative concentrations of sodium and potassium in the body.

Aromatization raises BP through the increased water-retention that accompanies the elevation in estrogen levels.

Nandrolone (a progestin) and methenolone (a DHT derivative) do not aromatize. As you mentioned, unlike most orals, oral methenolone is aceteylated rather than C-17 methylated, and so is very gentle on the liver.

Although neither compound is likely to increase blood pressure in the ways that oral and aromatizable compounds are able, both nandrolone and methenolone are potent erythropoietins.

In the case of methenolone (Primobolan), from what I see in the literature, erythropoiesis might be the only mechanism through which blood pressure could increase - it does not aromatize, and the oral is not C-17 methylated. Methenolone will thus neither increase estrogen nor act on the RAAS to change electrolyte levels. Furthermore, since it is so expensive, it is rarely ever used alone as a cycle - for most, the base will still be testosterone which is a potent erythropoetic on its own. If anything, the fact that methenolone is DHT-based could serve to diminish some level of aromatization and the water-retention due to estrogen, since DHT and DHT-derived compounds tend to act as aromatase inhibitors. But I'm just surmising. Those with more experience will surely speak up here.

Erythropoiesis increases blood pressure because the increase in red blood cell count stimulates the body to increase blood volume.

Summarizing:
  • Orals act through the RAAS.
  • Aromatizable compounds act through aromatase.
  • Non-aromatizable compounds act through erythropoiesis.

Did I get it right? What did I win? :)
 
Last edited:
Built said:
Anavar raises BP through RAAS-mediated upregulation of aldosterone, which changes the relative concentrations of sodium and potassium in the body.

Aromatization raises BP through the increased water-retention that accompanies the elevation in estrogen levels.

Nandrolone (a progestin) and methenolone (a DHT derivative) do not aromatize. As you mentioned, unlike most orals, oral methenolone is aceteylated rather than C-17 methylated, and so is very gentle on the liver.

Although neither compound is likely to increase blood pressure in the ways that oral and aromatizable compounds are able, both nandrolone and methenolone are potent erythropoietins.

In the case of methenolone (Primobolan), from what I see in the literature, erythropoiesis might be the only mechanism through which blood pressure could increase - it does not aromatize, and the oral is not C-17 methylated. Methenolone will thus neither increase estrogen nor act on the RAAS to change electrolyte levels. Furthermore, since it is so expensive, it is rarely ever used alone as a cycle - for most, the base will still be testosterone which is a potent erythropoetic on its own. If anything, the fact that methenolone is DHT-based could serve to diminish some level of aromatization and the water-retention due to estrogen, since DHT and DHT-derived compounds tend to act as aromatase inhibitors. But I'm just surmising. Those with more experience will surely speak up here.

Erythropoiesis increases blood pressure because the increase in red blood cell count stimulates the body to increase blood volume.

Summarizing:
  • Orals act through the RAAS.
  • Aromatizable compounds act through aromatase.
  • Non-aromatizable compounds act through erythropoiesis.

Did I get it right? What did I win? :)
Click to expand...

Thats probably a good guess IMO. But I still think it depends on the individual also. One person may can tolerate certain things better than others. It's all trail and error. But still, I will stand on my original statement......Methylated orals especially IMO will raise bp more and faster than say test E or C. I also think controlling bp from injectables by using something like Arimidex is easier. It gets more complicated with orals, just like built added.
 
Take the new compound Epistane for example...........when I used it, I started at 20mg/day for a week, went to 30 for a week then up to 40mg/day and my bp went sky high. Terrible headaches. I had to stop after 4 weeks. Nothing really I could do except stop cycle since this compound does not aromatize, but being methylated causes other unkown problems.
 
Built said:
Anavar raises BP through RAAS-mediated upregulation of aldosterone, which changes the relative concentrations of sodium and potassium in the body.

Aromatization raises BP through the increased water-retention that accompanies the elevation in estrogen levels.

Nandrolone (a progestin) and methenolone (a DHT derivative) do not aromatize. As you mentioned, unlike most orals, oral methenolone is aceteylated rather than C-17 methylated, and so is very gentle on the liver.

Although neither compound is likely to increase blood pressure in the ways that oral and aromatizable compounds are able, both nandrolone and methenolone are potent erythropoietins.

In the case of methenolone (Primobolan), from what I see in the literature, erythropoiesis might be the only mechanism through which blood pressure could increase - it does not aromatize, and the oral is not C-17 methylated. Methenolone will thus neither increase estrogen nor act on the RAAS to change electrolyte levels. Furthermore, since it is so expensive, it is rarely ever used alone as a cycle - for most, the base will still be testosterone which is a potent erythropoetic on its own. If anything, the fact that methenolone is DHT-based could serve to diminish some level of aromatization and the water-retention due to estrogen, since DHT and DHT-derived compounds tend to act as aromatase inhibitors. But I'm just surmising. Those with more experience will surely speak up here.

Erythropoiesis increases blood pressure because the increase in red blood cell count stimulates the body to increase blood volume.

Summarizing:
  • Orals act through the RAAS.
  • Aromatizable compounds act through aromatase.
  • Non-aromatizable compounds act through erythropoiesis.

Did I get it right? What did I win? :)
Click to expand...

Built, you're a star! :thumb: (Give me a few days to think of a suitable prize, will you?) You've added "RAAS-mediated upregulation of aldosterone" to my list of two mechanisms and that's very helpful. Two resulting actions from me:
1) I'll dig around and see if I can find more info on the degree to which individual compounds exhibit this as I haven't seen any discussion if it (on this forum or elsewhere) before;
2) I think I'm heading towards a Test E plus EQ cycle possibly with Primo tabs on top. I was concerned about the EQ being even more erythropotic (if that's the right word) than Test as people seem to rate that aspect of it highly (increaes appetite, stamina, etc) but if I swap out the Anavar then I may be ok here.

This is great stuff and exactly what I was hoping for.

Redflash
 
Well thanks - but I really just read a lot. If I overgeneralized or misrepresented any of these mechanisms, please let me know so I can update the post.
 
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