Does anyone know if EQ permantely raises blood pressure????
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Does anyone know if EQ permantely raises blood pressure????
No.
But if that was the case, who in their right mind would ever use it???
I know I sure would NOT!!!
~US~
You mean BP? No, it is not permanent. It can be due to a combination of factors, mainly increased erythropoeisis or polycythemia (increased production of red blood cells). The BP effects are sustained until the drug is withdrawn and the body has a chance to return to normal. Or you can intervene with meds or even draining blood (phlebotomy).
reading stupid threads raises bp
Androgens have a direct effect on blood pressure...it isn't due to increased erythropoeisis.Quote:
Originally Posted by ichabodcrane
All I know is it made mine go up while I was on then it went down slowly after the cycle though I won't know if it's back to normal til I see my doc next week.
What prompted the question?
This was brought up to me by a friend so I wanted to get everyone elses opinion on it. No way would i want EQ if it raised my bp permantely!!Quote:
Originally Posted by johnsomebody
thats cold...no b/p elavation is on only for a short time..will go back to normal after cycleQuote:
Originally Posted by asymmetrical1
I figured that when you go into talking about your BP and your overall health it is pretty important.
Why do you think I said it is due to a number of factors, mainly increased erythropoiesis? I wouldn't say that EQ is a strong androgen, nor that BP elevation is due mainly to the CNS stimulatory effects or estrogen conversion/salt and water retention. It is a known fact that increased red blood cell count can lead to excessive total intravascular volume and hence increased BP. So are you saying my statement is erroneous and that the increased BP one sees while on EQ is not due to polycythemia/erythrocytosis? Give me your reasoning!!!!!!!!!!Quote:
Originally Posted by longhornDr
bump
Hell, I can't even PRONOUNCE erythropoiesis!
This is pretty cocking coming from a newbie member. I don't know where you picked this up from but we don't do this here!! :no:Quote:
Originally Posted by asymmetrical1
As for the BP question ichabodcrane has given great advise. After you are done the cycle and your levels come back to normal your BP will return if you don't have any other underlining problems that cause Hypertension (high blood pressure)
I have encountered this and also remedied it with what you have said. Very true.Quote:
Originally Posted by ichabodcrane
What you said is erroneous. You give someone a high dose of any anabolic steroid and their BP will be elevated within hours....way too short of time for it to have anything to do with polycythemia.Quote:
Originally Posted by ichabodcrane
There is no correlation between hematocrit and blood pressure. I've done the studies.
So increased blood volume does not equal increased blood pressure? I know there are several mechanisms by which the body controls BP. If you think about the mechanisms by which AAS may increase BP they would be what? And fill in the ones I left out: but 1) RAAS- this is a maybe (the key system in controlling blood pressure and body fluid volume in pressure natriuresis) androgens may stimulate superoxides either directly or indirectly via effect on AngII on NAD(P)H oxidases. This would deplete NO leading to vasoconstriction. The combination of superoxide and NO = peroxynitrite, which oxidizes AA to produce F2-isoprostanes. The F2-isoprostanes are mediated by the thromboxane receptor, which may be upregulated by androgens, and would lead to vasoconstriction directly and indirectly by potentiating the vasoconstricor actions of AngII and stimulating endothelin production, which in turn may cause further renal vasoconstriction. 2) direct CNS stimulation (more for strong androgens?). They can pass the BBB and stimulate CNS by release of catecholamines-leading to vasoconstriction and increased CO. 3) Estrogen conversion and water retention. 4) Increased blood volume by increased erythropoiesis-longer process 5) Kidneys may contain AR's which affect Na+/H20 retention, kindof leading back to the RAAS. 6)The heart contains AR's which may affect contractility. LVH (left ventricular hypertrophy) has also been reported in chronic high dose AAS users. Again leading to increased cardiac output. 7) Also the effects of AAS and hypercholesterolemia-we know the effects in the long run. 8)** AAS effects on vascular smooth muscle-testosterone may provide vasodilatory effects which would be a plus. (http://www.brjpharmacol.org/cgi/cont...138/5/733#TBL2). Of course this must be dose related, and may prove against direct vasoconstriction as a mechanism for HTN. I am sure this is not all of them and some mechanisms may overlap eachother. Also, these mechanisms include both direct and indirect actions and can be time/dose related.Quote:
Originally Posted by longhornDr
Anyways, we know EQ is not a strong androgen. So I would rule out CNS stimulation, at least in part. We know EQ does not convert to estrogen much in moderate doses so I would rule out estrogen conversion. It is not a strong androgen, so I am not sure what effect exactly it would have on the RAAS or heart contractility. I have not witnessed increases in BP until later on in EQ cycles, also leading me to believe increased RBC may be a primary mechanism. I do know that increased red blood cell production is a given when taking EQ. People witness incredible pumps, and vascularity further leading me to the conclusion that inreased erythropoiesis is playing a key factor here.
As far as hematocrit and blood pressure, sure there is a correlation. As hematocrit increases so does blood volume and blood viscosity. If you think about the major ADE's we worry about when giving somenoe rEPO (for whatever reason), it is mainly hypertension due to volume overload and clotting disorders due to increased viscosity.
I am not saying that there aren't other mechanisms involved in HTN when using EQ. But I believe (and of course this is my opinion) that increased blood volume is the major factor when using EQ. Have you ever used it alone? I have, and I didn't witness an increase in BP until the EQ started kicking in. This was followed by the insane pumps and vascularity which EQ is notorious for. I don't want to start a conflict and didn't mean to sound that way, but I am just curious about your point of view on this and what mechanisms you feel attribute to the HTN associated with EQ use?
Bump for Ichabod.
You have to read his post slowly to make any sense of it..wow. Ichabod I have a question for you: how much volume do you think is actually increased by the additional red blood cells? I think it would have to be a substantial amount to increase blood pressure..
In lieu of Ichabod's answer I'd recommend anybody concerned about their BP while on EQ to get a BP monitor at a drug store. They're not all that pricey though you'll probably have to get an oversized cuff as well.
Excellent post bro! I also am convinced that the renin-angiotensin-aldosterone system is affected tremendously by certain synthetic androgens (dbol for example). Very good call on this explanation even if it doesn't directly apply to EQ as much as the increased blood volume explanation.Quote:
Originally Posted by ichabodcrane
Does EQ increase BP via haematocrit or blood volume? i have seen cases where a higher than average crit has been noted, without an increase in BP.Quote:
Originally Posted by ichabodcrane
An increase in RBC count would increase the crit, but it IS possible to increase the crit without increasing overall blood volume.
What mechanisms are present to control the blood volume where a crit increase is seen?
curious:scratch:
Yeah, its REAL simple to use -I was surprised. It inflates and deflates itself automatically, then gives you the readout. All you have to do is strap it on and push "go". The manual explains the numbers, which was great since I didn't have a clue either til I read the thing. That alone was about worth the price.Quote:
Originally Posted by SGFuryZ
Sorry for the delay, we just gave birth to my new son Wed. So it is hard for me to continue this thread. Anyways:Quote:
Originally Posted by halifaxsteve
Actually you pose a good question. You can and do see an increased Hct w/o an overall increase in plasma volume. In fact according to the equation Hct=red cell volume/total blood volume, you would expect an increase in Hct with a decrease in blood volume. Or Hct rises when the # of RBC's rises or when blood volume is reduced. People who smoke, high altitude dwellers, people with COPD, or people with any kind of hypoxia generally have a higher Hct. But this doesen't always mean they will have a high BP. Hct is just the measurement of the proportion of blood that is made up of red blood cells and is expressed as a fraction of percentage of cells in the blood, ie. #of RBC's/100mL of blood. But if you consider someone with polycythemia vera (I am not saying this is what happens with EQ usage, but just consider it. I maybe should not have used the word polycythemia so "freely"?), they generally have complications due to expanded blood volume and viscosity (red skin spots-bruising, erythema, fatigue etc.) Hct is elevated. The increased viscosity causes increased pressure against vessel walls and ultimately causes increased CO which can increase BP. Aside from this, the body usually has multiple mechanisms where it compensates for increases/decreases in BP. Where one mechanism is lacking, another is closely behind to fill its place. Just like we see when we give someone diuretics for HTN, eventually the low BP will trigger other mechanisms to try and increase BP (increased CO, etc.) So I am not sure, but maybe we are forcing the production of RBC's and this leads to increased volume, along with other mechanisms being blunted or overstimulated? When we give people EPO, we also see increased Hct and we monitor for hypertension and clotting disorders. I have read many studies stating that the increase in Hct is not related to HTN, but just as many stating otherwise. ex: http://www.medscape.com/viewarticle/449738_4 (requires medscape free signup). Just a case report but worth the read anyways.
Also, some people never witness increases in BP when using any AAS, while others do even using minor doses of very mild substances. I am sure there are many mechanisms involved, as well as compensatory mechanisms. But I have witnessed first hand the increased Hct, followed by HTN when using EQ. It took several weeks to manifest, also leading me to conclude that increased blood volume was a factor here. What are your opinions?
Hell, sounds good to me!
And CONGRATULATIONS ICHABOD!!!
firstly, i don't believe that 'any' anabolic steroid would cause a spike in bp w/in hours. deca, or another esterified steriod would not cause a spike in blood pressure immediately. the only thing which could cause a rapid spike would be something like suspension, or fast acting oral anabolic.Quote:
Originally Posted by longhornDr
i belive that a rapid increase in erythropoeisis can cause transient hypertenstion, but it's not "the" causitive agent. i am not well versed in this area, but i am sure that there are compensatory mechanisms to deal with an increased crit. i belive the true cause of hypertenstion to be a combination of many mechanisms at work, as ichabod mentioned.
i am curious however...with EQ usage, erythropoeisis is known to occur. but by how much does the crit increase, and has anyone ever measured the overall blood volume? is the blood volume just a theory or a well researched, scientific fact?
congrats on the newborn incabod! :)
Thanks guys! It was cool. My third child, so lots of work to do on top of school. But Halifax, do a search on medline/pubmed and you will find that AAS do infact increase blood volume. There are numerous proposed hypothesis by which AAS increaese BP. But wouldn't you think that the incredible pump and vascularity would be key signs of increased volume? People who take EPO get HTN all the time. Yes the body does have methods for compensating for this. But if you are forcing erythropoeisis, increasing blood volume surely follows, increased CO pursues as well + many others. If you took a normal person and put them at a high altitude, you would expect to see an increased crit and blood volume. The body would soon adjust to this through compensatory mechs. But I think we are forcing an increase in blood volume, beit from increased EPO (which I do think happens) or through increased plasma volume by increased Na+/H20 retention by effect on renal tubular cells, or both. I could not find primary lit on boldenone specifically and HTN, but I could on other AAS. But I just don't see why an increase in RBC's leading to increased overall vascular volume would not lead to HTN. Maybe we are not able to compensate because the AAS in question is blocking the mechanism of compensation? Or adding to it? But increased blood volume would lead to increased BP. I know and have witnessed increased Hct, pumps, vascularity (volume?) during EQ usage as well as other people. So help me figure out the true mechanism if I am wrong because I really want to know as well. I don't consider EQ to be a strong androgen, so this is why I rule out some of the other mechanisms. EQ does not aromatize in moderate dosages much, so I ruled out this mech as well. I don't get all puffy and bloated on EQ, and I don't feel the CNS effects like I do on d-bol. So, hmmm?Quote:
Originally Posted by halifaxsteve