Controlling Acute Hypertension from Exogenous Hormones

[AlphaLife]

I am 31, 5'10, and 190 lbs at about 10% BF. I have run 6 cycles in the past. I have never noticed any symptoms of HTN before my most recent (currently ending) cycle: test e (150mg e3d), tren e (200 mg e3d), mast for 4 weeks (300mg e3d), ending with test ph (100mg ED), tren a (150mg EoD), and NPP (150 mg EoD).

A few times in the last couple weeks of my 12 week cycle I have experienced relatively intense pain in my upper left neck. It feels like I slept wrong or like a headache is creeping in. I decided to test by BP with a home monitor device and have been in the 150-160/90-100 range on a few occasions. I was taking sibutramine and decided to d/c it as I thought that may be the culprit (never experienced HTN before on cycle). Unfortunately, the HTN remained.

I understand this is temporary and will subside when my cycle ends, but it is concerning for a variety of reasons, including long-term health implications and interfering with my ability to work out.

I have done a good amount of research on this, which is to say I spent a few days looking into forum posts on the topic and reading NIH studies on BP meds as well as evaluating side effects etc via drug profiles.

Of course, I first tried what I had "on hand." I have had issues with pre-gyno symptoms the last two cycles so I was running Aromasin at 12.5 mg/ED and Nolva at 10mg/ED which was doing well at eliminating/preventing swelling and sensitivity. My initial hypothesis was that my E2 was high resulting in water retention and constricting my blood vessels resulting in increased BP. So I decided to increase Aromasin from 12.5mg ED to 25mg ED. I kept Nolva at 10mg/day. That did not alleviate the HTN so I tried to eliminate the water retention with Aldactone. I just ran it for 2 days at 50mg 2x/day, but that also did nothing--except I did get muscle cramps which I could not treat with potassium d/t the interaction with Aldactone.

The options I have found via research that seem most appealing are these:

1. Combination of celery seed and hawthorn extract--not sure this will actually work, although I am willing to try.
2. Telmisartan--sounds ideal.
3. Hydrochlorothiazide--not confident in this as Aldactone didn't work, but at least I could treat/prevent cramps while taking it.

What are your thoughts? Experiences?

Thanks for your input.

 

[Big_paul]

If you are running a cycle the best you can do is keep bp somewhere close to normal with medication because hormone levels are just whacked. You will be high or low. If you are off cycle and your bp is still high, you can treat it with medication successfully, it is almost impossible to dial it in on cycle though.

 

[weighted chinup]

Blood pressure medication is some of the most commonly prescribed medications there is. There is no reason to self medicate on your own when a doc can do it for you. Take advantage of the fact they know treating BP extremely well.

That is my recommendation.

 

[Docd187123]

BP issues on cycle are not due to estrogenic effects. It's from the AAS itself therefor no amount of estrogen control will help with HTN to any significant degree. You'll either have to reduce the dose of the offending compound/s, cut the cycle short, or medicate.

 

[penche]

Hydrochlorothiazide I've tried when my BP was up, didn't work for crap.

I use a low dose of carvedilol(6~9mg) if mine acts up.
lisinopril Is another common BP med. Consult with your doc tho.

 

[Roger rabbit]

Don't forget about Cialis[emoji16]
5mg daily can help to reduce blood pressure.

Also, back to basics here.
Are you drinking plenty of water? Thick blood will raise blood pressure.

Have you had bloods done to check out your hemocrit? Again, goes back to thick blood and you are running a good amount of gear, pair that will being slightly dehydrated and you will elevate your blood pressure.

O


Sent from my iPhone using Tapatalk

 

[Brandaddy]

Good old cialis, cardio, and water bud.

 

[AlphaLife]

Don't forget about Cialis[emoji16]
5mg daily can help to reduce blood pressure.

Also, back to basics here.
Are you drinking plenty of water? Thick blood will raise blood pressure.

Have you had bloods done to check out your hemocrit? Again, goes back to thick blood and you are running a good amount of gear, pair that will being slightly dehydrated and you will elevate your blood pressure.

O


Sent from my iPhone using Tapatalk

I'm planning to get end of cycle bloodwork done this weekend. Mid-cycle wasn't having this issue. I am definitely interested in a few of these numbers.

I could definitely do better on water intake. I know that's a factor. I need to better commit to that for sure.

Thank you for the feedback bro.

 

[AlphaLife]

Good old cialis, cardio, and water bud.

I do cardio. Not much. Usually somewhere between 15-30 minutes per day, but I do cardio most days.

Thank you for the feedback bro.

 

[AlphaLife]

Hydrochlorothiazide I've tried when my BP was up, didn't work for crap.

I use a low dose of carvedilol(6~9mg) if mine acts up.
lisinopril Is another common BP med. Consult with your doc tho.

Thank you for the feedback. I do think I need to get an MD that I can talk to about this. I don't want to use my usual GP because if I need to send medical records to some government agency, court, etc, I don't want any mention of this in there. I think I am going to establish a relationship with a second GP for this specifically.

 

[AlphaLife]

BP issues on cycle are not due to estrogenic effects. It's from the AAS itself therefor no amount of estrogen control will help with HTN to any significant degree. You'll either have to reduce the dose of the offending compound/s, cut the cycle short, or medicate.

Thank you for your response Doc.

Respectfully, I was under the assumption based on what I had read here and elsewhere that too much E2 increased water retention (bloat) which constricts your blood vessels, requiring your heart to pump harder (increase blood pressure) to maintain normal flow. I don't really think that is my problem necessarily as I don't look bloated, but I didn't think it was out of the question as a source of the problem.... Is there some literature you could direct me to that disproves this theory?

Always learning,

AL

 

[Docd187123]

Thank you for your response Doc.

Respectfully, I was under the assumption based on what I had read here and elsewhere that too much E2 increased water retention (bloat) which constricts your blood vessels, requiring your heart to pump harder (increase blood pressure) to maintain normal flow. I don't really think that is my problem necessarily as I don't look bloated, but I didn't think it was out of the question as a source of the problem.... Is there some literature you could direct me to that disproves this theory?

Always learning,

AL

Here is a post by Dr. Scally from a while back.

Re: A HOW TO for: SERMs, Aromatize inhibitors, Gyno and PCT *A must read








This is getting off-topic from the OP, but since E2 has been stated as causing "bloat," which is then the cause of PB [sic] problems, I will address this in a brief manner. "Newly" found elevated BP after administering AAS can be a challenge to the user as well as the caretaker.

The simple idea that this problem arises from E2 is without supportive evidence. I came to this conclusion very early in treating AAS users by the fact that no amount of E2 control managed the BP. I am sure this is the experience of many AAS users. This is further confirmed by the fact that non-aromatizable AAS can cause elevated BP. [Proviron is reported to cause an increased BP.] This observation would lead one to conclude that the AAS itself is the source of the BP problems and lowering E2 while AAS are high will have limited success.

As the elegant study below shows, androgens (Testosterone) do appear to be the cause. I have never argued against E2 control, but directed therapies at their cause, thus SERM for gynecomastia. In the clinical context where an AI is being used for E2 control and BP is a problem do not look at more AI to further lower E2, but treat the BP.


The researchers present new evidence on genomic and nongenomic mechanisms of testosterone action on vascular smooth muscle cells in arterial hypertension through modulating associated cellular events, thus setting the stage for further aggravation of hypertension. Using animal models of normotension and polygenic hypertension, the investigators found that, in vascular smooth muscle cells from male animals, testosterone regulates cellular processes, which mediates vascular contraction and hypertrophy, key events contributing to the increased vascular resistance in hypertension. They also observed greater production of reactive oxygen species in response to testosterone in vascular smooth muscle cells from hypertensive as compared with normotensive animals. These effects were not attributed to conversion of testosterone to 17Beta-estradiol, because the aromatase inhibitor anastrazole had no effect on reactive oxygen species formation.


Barton M, Prossnitz ER, Meyer MR. Testosterone and Secondary Hypertension: New Pieces to the Puzzle. Hypertension. Testosterone and Secondary Hypertension


Chignalia AZ, Schuldt EZ, Camargo LvL, et al. Testosterone Induces Vascular Smooth Muscle Cell Migration by NADPH Oxidase and c-Src-Dependent Pathways. Hypertension. Testosterone Induces Vascular Smooth Muscle Cell Migration by NADPH Oxidase and c-Src–Dependent Pathways

Testosterone has been implicated in vascular remodeling associated with hypertension. Molecular mechanisms underlying this are elusive, but oxidative stress may be important. We hypothesized that testosterone stimulates generation of reactive oxygen species (ROS) and migration of vascular smooth muscle cells (VSMCs), with enhanced effects in cells from spontaneously hypertensive rats (SHRs). The mechanisms (genomic and nongenomic) whereby testosterone induces ROS generation and the role of c-Src, a regulator of redox-sensitive migration, were determined.

VSMCs from male Wistar-Kyoto rats and SHRs were stimulated with testosterone (10?7 mol/L, 0–120 minutes). Testosterone increased ROS generation, assessed by dihydroethidium fluorescence and lucigenin-enhanced chemiluminescence (30 minutes [SHR] and 60 minutes [both strains]). Flutamide (androgen receptor antagonist) and actinomycin D (gene transcription inhibitor) diminished ROS production (60 minutes). Testosterone increased Nox1 and Nox4 mRNA levels and p47phox protein expression, determined by real-time PCR and immunoblotting, respectively. Flutamide, actinomycin D, and cycloheximide (protein synthesis inhibitor) diminished testosterone effects on p47phox. c-Src phosphorylation was observed at 30 minutes (SHR) and 120 minutes (Wistar-Kyoto rat). Testosterone-induced ROS generation was repressed by 3-(4-chlorophenyl) 1-(1,1-dimethylethyl)-1H-pyrazolo[3,4-day]pyrimidin-4-amine (c-Src inhibitor) in SHRs and reduced by apocynin (antioxidant/NADPH oxidase inhibitor) in both strains. Testosterone stimulated VSMCs migration, assessed by the wound healing technique, with greater effects in SHRs. Flutamide, apocynin, and 3-(4-chlorophenyl) 1-(1,1-dimethylethyl)-1H-pyrazolo[3,4-day]pyrimidin-4-amine blocked testosterone-induced VSMCs migration in both strains.

Our study demonstrates that testosterone induces VSMCs migration via NADPH oxidase–derived ROS and c-Src–dependent pathways by genomic and nongenomic mechanisms, which are differentially regulated in VSMCs from Wistar-Kyoto rats and SHRs.

 

[AlphaLife]

Here is a post by Dr. Scally from a while back.

Thanks Doc!

 

[AlphaLife]

Here is a post by Dr. Scally from a while back.

I suppose that eliminates option 3, Hydrochlorothiazide. Honestly, it was option 3 because I didn't think it would help based on the failure of increased Aromasin and addition of Aldactone to reduce my BP.

I really appreciate the scientific response to my question.

 

[Docd187123]

I suppose that eliminates option 3, Hydrochlorothiazide. Honestly, it was option 3 because I didn't think it would help based on the failure of increased Aromasin and addition of Aldactone to reduce my BP.

I really appreciate the scientific response to my question.

Not necessarily bc while E2 causing water retention leading to HTN isn't the chain events, it doesn't mean BP meds won't help.

 

[AlphaLife]

Not necessarily bc while E2 causing water retention leading to HTN isn't the chain events, it doesn't mean BP meds won't help.

Okay. But wouldn't Telmisartan be better for a number of reasons? Seems to have multiple benefits and not too strong. Then again, I should see an MD.

What BP meds would you recommend for PRN use?

 

[Docd187123]

Okay. But wouldn't Telmisartan be better for a number of reasons? Seems to have multiple benefits and not too strong. Then again, I should see an MD.

What BP meds would you recommend for PRN use?

I'd see your doctor and let him supervise treatment should you need it.

I have never suffered from high blood pressure and never looked muh into this class of drugs so I'm uneasy ahit offering up a recommendation. I'd just see your doctor.

 

[AlphaLife]

I'd see your doctor and let him supervise treatment should you need it.

I have never suffered from high blood pressure and never looked muh into this class of drugs so I'm uneasy ahit offering up a recommendation. I'd just see your doctor.

Understood. Thank you.