Clen headaches

[Lemonada8]

Christ I wasnt gonna , but I cant help it. It can when there is an increase in contractile force and heart rate. Just like when you exercise there einstein. vasodilation occurs...but there is an increase in heart rate and contractile force therefore an increase in BP. Now please STOP!

Thank your for mentioning that its similar to the increase in BP during exercise. Yet, when u exercise u have an increase in venous return because of the muscle contraction and decreased pressure in the thoracic cavity via increased respirations; along with the constriction of non-essential vessels (ie messentaric) Also, remember that initially there is a drop in BP at the start of exercise which then increases.

So, with the case of using Clen. It is a vasodilator, so you get the vasodilatory effects which lowers resistance, then yes the increased contractilty and HR help maintain CO. BUT, where does the increased venous return come from? there is no exercising muscle to help return blood flow to the heart (increase EDV), and no sympathetic output to vasoconstrict the non-essential vessels ( they would actually dialate, further decreasing resistance). Even if the compensatory reflex release of sympathetics vasoconstricts those arteries, there is no muscular activity to increase venous return (EDV). So how does EDV (end diastolic volume) increase? * thats the real question, that i was trying to ask, but noone really got that.
So, an increase in Contractility and HR wont ( actually over compensate) for the decrease in TPR following taking clen.

BP = CO x TPR
CO = SV x HR
SV = EDV-ESV ( assuming no regurg)
Preload is basicaly the same as EDV

Hell of a lot of trouble just so you dont have to be wrong.
Ive seen it before (in all of places another clen thread in fact). yea, when i was just tryin to say how cardiac changes could occur with clen usage. which was finally noticed at the end by swifto and it really comes down to how it is bein used.
Wouldnt it be easier just to say , yeah it probably is because the heart is contracting with more force and more rapidly.
Just sayin ...christ ....

[jimmyinkedup]

.............................

[Lemonada8]

.....................

no point to keep one side of a spat.

[jimmyinkedup]

^^ You are entitled to your opinion there Lemon.
Oh and btw mean arterial pressure increases with pulse pressure.
Your wrong.

[Lemonada8]

Mean arterial pressure = 1/3 systolic pressure + 2/3 diastolic pressure
Pulse pressure = Systolic pressure - diastolic pressure

that statement doesnt make sense.
what exactly am i wrong about? I dont see your point.
An increase in pulse pressure is a widening of the gap between SBP and DBP.

and i dont think i talked about MAP and PP...

[stevelifts]

Mainly on the arterioles ( i was mistaken in an earlier post), thats where primarily the beta 2 receptors are located



correct, i was aiming towards clen puts the body in the artificial state of hypovolemia, which then the response mechanism kicked in. Ultimately its due to the increase in blood volume(in response to the initial 'shock' of hypovolemia, which was due to the decrease in afterload resistance; sensed by the carotid body as decreased stretch), and the beta 2 activation in the kidney which increases the release of renin, which continues to increase blood volume.

Then headaches were caused by the hyperosmolarity of the plasma, but when that restabalized they went away which lowered the ADH secretion, which slowed fluid retention (via ADH) but the RAAS is still going due to the renin release

It is primarily beta 1 that effects renin and Aldostrone and ATII . Not beta 2.

[Lemonada8]

It is primarily beta 1 that effects renin and Aldostrone and ATII . Not beta 2.

It differs in different books... But primarily they say beta 1. I agree with that minor difference. If its not a direct stimulation then it would be a compensatory activation resulting from the use of clen (which I have already discussed previously)




Another question, when u r done using clen do u piss like a race horse?
If so, that would support my claim of increased claim of blood volume because when the vasodilation stimulation is removed the compensatory blood volume increase is no longer needed so it's removed from the body.

The higher blood volume is the response to the decreased stretch
the velocity increases linearly due to decreased resistance which would decrease the transmural pressure (decreasing the stretch on the carotid body, which would initiate the compensatory response of increasing blood volume)
And with an increased blood volume and increased linear flow the measurement of BP would increase.
Think like this way: if there is more volume in the vessel, the way BP is measured is compression of the artery from an external source. If there is more volume being compressed for the BP measurement then it would take a higher pressure to fully compress the vessel to achieve the same korotkoff sounds used to determine the BP.

[AD]

Lemon. Your explanation is vasodilation triggers fluid retention and that raise bp. Is that correct?

so let say due to some unfortunate event, you're in shock. could be hypovolemic, could be septicemic, could be anaphylactic.. something. would you like to be treated immediately with a vasodilator to boost your blood pressure?

[AD]

It differs in different books... But primarily they say beta 1. I agree with that minor difference. If its not a direct stimulation then it would be a compensatory activation resulting from the use of clen (which I have already discussed previously)

how many "minor difference" have we had now... maybe you shouldn't say you're pretty damn good.

[stevelifts]

It differs in different books... But primarily they say beta 1. I agree with that minor difference. If its not a direct stimulation then it would be a compensatory activation resulting from the use of clen (which I have already discussed previously)

Its not different anywhere. b1 receptors mediate the release/secretion of renin. The "compensatory activation" as you refer to it from use of a b2 agonist such as orally administered clen or albuterol would hardly be sufficient to be solely responsible for the hypertensive state. Even less so for an inhaled b2 agonist such as salmeterol.
I am scratching my head wondering why you are looking at obscure, less than likely secondary effects when the answer is string you right in the face(and has been pointed out) ??

[Bonaparte]

Its not different anywhere. b1 receptors mediate the release/secretion of renin. The "compensatory activation" as you refer to it from use of a b2 agonist such as orally administered clen or albuterol would hardly be sufficient to be solely responsible for the hypertensive state. Even less so for an inhaled b2 agonist such as salmeterol.
I am scratching my head wondering why you are looking at obscure, less than likely secondary effects when the answer is string you right in the face(and has been pointed out) ??

Because that would involve humility.

[Noles12]

Can I borrow the ruler to measure my dick next?

[Swifto]

Its not different anywhere. b1 receptors mediate the release/secretion of renin. The "compensatory activation" as you refer to it from use of a b2 agonist such as orally administered clen or albuterol would hardly be sufficient to be solely responsible for the hypertensive state. Even less so for an inhaled b2 agonist such as salmeterol.
I am scratching my head wondering why you are looking at obscure, less than likely secondary effects when the answer is string you right in the face(and has been pointed out) ??

We have a winner!

I'm afriad this is a common trait of Lemon's. He's done it many times before and will continue to do it.

Its nice watching him squirm though.

Thank-you for your contribution.

[Swifto]

I guess its time to post this, which I was sitting on.


Clin Exp Hypertens A. 1983;5(2):225-38.

Subclassification of human beta-adrenergic receptors mediating renin release.

Weber F, Brodde OE, Anlauf M, Bock KD.
Abstract

To determine the beta-adrenoceptor subtype controlling renin release from the kidneys, several beta-adrenoceptor subtype selective agonists and antagonists were administered to 15 healthy volunteers. While isoprenaline infusion (1, 2 and 4 micrograms/min for 5 min each) markedly increased plasma renin activity (PRA), the beta 2-selective agonist fenoterol failed to change PRA. The isoprenaline induced rise in PRA could be completely prevented by the beta 1-selective antagonists metoprolol (10 mg i.v. 45 min prior to isoprenaline infusion) and betaxolol (5 mg i.v. 45 min prior to infusion) indicating that renin release is mediated by beta 1-adrenoceptors. Binding studies with the highly specific beta-adrenoceptor radioligand (+/-)-125iodocyanopindolol demonstrated that membranes from human kidney cortical slices contain predominantly, if not exclusively, beta 1-adrenoceptors. These in vivo and in vitro results support the view that the beta-adrenoceptor mediating renin release from the human kidney is of the beta 1-subtype.


Here you go now, on some wild theory why its incorrect...

[warmouth]

I cant believe I was avoiding this thread. I saw 3pages worth and had to check it out. Very informative!

[Lemonada8]

Lemon. Your explanation is vasodilation triggers fluid retention and that raise bp. Is that correct? 1

so let say due to some unfortunate event, you're in shock. could be hypovolemic, could be septicemic, could be anaphylactic.. something. would you like to be treated immediately with a vasodilator to boost your blood pressure? 2

1) Yes, in a very generic sense.
General physio real quick.
Beta-2 will increase cAMP in smooth muscles. This will phosphorylate the MLCK complex which will decrease the contraction strength of the smooth muscle.
Alpha-1 will increase the Ca2+ influx into cells, which will increase the strength of the contraction in smooth muscle.
The continuous vasodilation will trigger fluid retention naturally by the body; however it doesnt occur immediately. It will take time and increased fluid intake to fully compensate for the decreased resistance back to a hemodynamic homeostasis. Clen will decrease the normal 'tone' of the vascular smooth muscle by increasing cAMP in the cells, phosphorylating the MLCK complex which decreases the availability of Ca2+ to bind resulting in a contraction. Thats why when the compensatory effects of the sympathetic system hitting the Alpha-1 receptors, it cant cause enough Ca2+ to enter the cell to constrict the vascular smooth muscle to compensate for the dilation (relaxation) but in the other cells (where Clen isnt bound, increasing the cAMP in those cells) will clamp up hard to compensate for the loss in resistance. This also will happen in the venous side of the vessels to help increase the return of blood to the heart (along with the increased HR). The loss in resistance will affect afterload (So the blood needs less force to travel throughout the body) But to only decrease afterload without affecting preload will result in the heart contracting but having a severely decreased stroke volume will result in a massive drop in cardiac output which an increase in HR cant fix. That, combined with Frank-Starling mechanics (in cardiac muscle, if u stretch out the muscle it will contract stronger; up to a point), the decrease in afterload with no change in preload would result in less contractility of the heart. So to fix this, the veins will vasoconstrict (remember that ~70% of the today blood volume resides in the veins) which will temporarily increase the amount of blood returning to the heart (aka preload, the stretch of the chamber before a contraction) which acutely compensates for the sudden decrease in resistance. But the vasoconstriction of the veins is not a specific thing, its a systemic effect but to continuously have those sympathetics fire will result in other actions in the body (the kidney for instance). Since the 'unnatural' decrease in resistance is induced by clen intake, it results in an increased blood volume over time because of the increased sympathetics to the kidney, hitting the Beta 1 receptor, resulting in fluid retention. This is also the reason for the massive increased urination after stopping clen, the fluid is no longer needed in the same quantity so its excreted from the body.
The headaches (back to the initial topic) are a side effect of the sudden onset of the sympathetic response, which will vasoconstrict the vessels not already dilated by the clen usage, and other sympathetic responses from the body. Then with the continued use of Clen, which keeps the resistance down, which continues the keep the sympathetics firing, which triggers fluid retention from the kidneys; results in a hyperosmotic state (because of not enough water intake, and the kidneys trying to increase fluid volume by absorbing sodium). Which in a hyperosmotic state, ADH is secreted which reabsorbs water but is also a vasoconstrictor; to help resolve the problem of high olsmolarity. This is shown to be accurate because of the 'cure' (drink lots of water and supplement taurine). Drinking lots of water will help lower the osmolarity of the blood because it is absorbed, which slows down the kidneys reabsorption of sodium. The taurine helps with osmotic balance between the cells and the blood. When the blood becomes either hyperosmolar or hypoosmolar, taurine helps keep the cells from the osmotic effects of the blood. Since it is a sudden increase in osmolarity in the blood plasma, the taurine runs out quickly in the cells (not talking about RBC's, but other cells). So by supplementing taurine, it replenishes the taurine lost in the cells which helps maintain balance. This combined with increased water drinking helps bring back the osmolar balance in the blood, and increasing the blood volume which lowers the sympathetic response to the loss in vascular resistance which was due to the continuous use of clen.
yet this is the non-acute resolution and how it creates increased BP with time. The reason there is an acute increase in BP, is the sympathetic response, which has the vasoconstriction effects systemically until the body can fully compensate for the change and not have to keep firing to maintain balance.

2) No. If it is a natural cause of shock due to some event don't give a vasodilator because it will not act fast enough to compensate for the loss in fluid. The solution for those types of shock is basically give fluids and treat the underlying cause of the shock. If anything, give a vasoconstrictor to help increase the resistance of the vessels to bring back balance to the hemodynamics. Also, since it is not due to constant use of a drug but more of an event there wouldn't be the continuous effect maintaining the 'shock'.

how many "minor difference" have we had now... maybe you shouldn't say you're pretty damn good.

Beta 1 vs beta 2 receptors is a very minor difference, its both sympatetics. And the fact that it really doesnt change the fact of what i was saying and how the compensatory effects occur, its its a minor thing.

Its not different anywhere. b1 receptors mediate the release/secretion of renin. The "compensatory activation" as you refer to it from use of a b2 agonist such as orally administered clen or albuterol would hardly be sufficient to be solely responsible for the hypertensive state. Even less so for an inhaled b2 agonist such as salmeterol.
I am scratching my head wondering why you are looking at obscure, less than likely secondary effects when the answer is string you right in the face(and has been pointed out) ??

The compensatory activation is due to the ORAL clen use. Albuterol is short acting, so the effects that it has arent nearly as long lasting, and inhaled salmeterol is more direct towards the lungs because of the mechanism of administration.
That combined with what ive already said, and its a higher dose than necessary for its original actions; has to result in what ive been saying. Clen at LOW DOSES (or therapeutic doses) will LOWER BP, period. The fact that people take much higher doses compared to the therapeutic dose is what triggers the compensatory activation. The increase in HR and contractility alone from the B2 agonist is not nearly enough to explain the end result. But thanks for responding, although all you have said is that what im saying is obscure and 'less than likely secondary effects' are basically wrong, without actually replying to anything ive said minus the " its beta1 in kidney, not beta 2" and i should just accept what others have said; yet NOONE has actually commented on the full aspect of what ive been saying (with the exception of Asiandude, who actually has been a real contributor in this debate/discussion).

Because that would involve humility.

Dont even start Bonaparte. I have humility, i admit when im wrong; or i say something thats incorrect. But only when its actually done; and had stuff to back it up. Not just keep repeating the samething over and over again; especially when I have already replied to that notion with a rebuttal debating reply; and all that is responded to that is "no, you are wrong, I am right" and just trying to say it louder.

We have a winner!
I'm afriad this is a common trait of Lemon's. He's done it many times before and will continue to do it.
Its nice watching him squirm though.
Thank-you for your contribution.

I guess its time to post this, which I was sitting on.
Here you go now, on some wild theory why its incorrect...

And Mr White Knight comes in to save the day and sound perfectly correct and try to insult me. First off, dont lie that you have 'been sitting on a study' which shows i was wrong about one MINOR detail, which has nothing really to do with the whole compensatory effect of my debate. You found one minor thing, and with that i am completely in the wrong? Hmm.. Ill use a quote from someone already in this thread "only thing that matters is some potentially flawed study on pubmed dealing with receptor binding affinities which can be optimistically translated into real world results through a MENTAL DETACHMENT FROM REALITY".
And how am I squirming? Because i have to repeat myself over just to try to get an actual intelligent ( or legitimate response pertaining to the discussion, not just insults and 'shut ups')
And Common trait? Ill take that as a compliment because it was a debate, where i never just gave blatant insults but actually intellectually responded to what I was getting for responses. So, Thanks. I can debate without getting upset ( minus this post, cuz its pathetic), and actually have intelligent responses where i respond to all aspects of the original comment.

^^ You are entitled to your opinion there Lemon.
Oh and btw mean arterial pressure increases with pulse pressure.
Your wrong.

And with this... Seriously? How f-in childish it this post. You post a snarky post aimed towards me, and I respond to it; then you go and delete what you said then post a response basically making it look like i came out of nowhere with that insult and you are the 'good hearted' person by giving me the 'entitled opinion' bullsh*t? That is freakin childish. Grow up. And yes, we did have a debate ( if it can actually be called that) because all you ended up doing was repeating yourself louder and accompanying that with insults all-the-while, never actually replying to what i was saying. And funny thing is that all it started out was, i was trying to say "how" some of those issues could occur, and what they were. Not that they actually did every time; but more going with the physiological approach on how that danger occurred.


Here, since noone here really knows how to debate and have an intelligent discussion; and just likes to say 'you are wrong, and shut up' without actually ever replying to what ive been saying. Read this http://commfaculty.fullerton.edu/jbr..._academic_.htm Its an article on HOW to debate and such. But dont try and quote me on stuff, i just scanned over it and it looked pretty informative since it seems people are out of touch on how to debate.
Real life example: the Romney/Obama Debate. Who won? Romney. Who Kept repeating themselves, never addressing what was being said, and actually got frustrated? Obama.
See a resemblance here somewhat to this attempted debate here?

Thanks and have a good day.

[Phased]

I hope you had a nice glass of Lemonade after that Titanic post

[AD]

2) No. If it is a natural cause of shock due to some event don't give a vasodilator because it will not act fast enough to compensate for the loss in fluid. The solution for those types of shock is basically give fluids and treat the underlying cause of the shock. If anything, give a vasoconstrictor to help increase the resistance of the vessels to bring back balance to the hemodynamics. Also, since it is not due to constant use of a drug but more of an event there wouldn't be the continuous effect maintaining the 'shock'.

may i know what is the time frame for this to actually happen?

what is the usual time frame after a first dose of clen for users to start feeling increase in heart rate and blood pressure?

any idea what is the expected magnitude of bp correction after using a vasodilator? back to normal? 10mmHg above normal? 50mmHg above normal? what is the mechanism that stops this rebound from going into malignant hypertension?

[Lemonada8]

may i know what is the time frame for this to actually happen?
what is the usual time frame after a first dose of clen for users to start feeling increase in heart rate and blood pressure?
any idea what is the expected magnitude of bp correction after using a vasodilator? back to normal? 10mmHg above normal? 50mmHg above normal? what is the mechanism that stops this rebound from going into malignant hypertension?

The kidneys take about 2-3 days to get rolling with compensation provided adequate hydration and taurine supplementation.
As for the degree of change, that depends on the person and the dosage and how their hydration status is when starting Clen.
I wouldn't consider this malignant hypertension because it is induced by taking Clen at high doses and when that can be balanced out then the Bp should drop from the initial raise which resulted from the immediate compensation.
If I had to put a time frame from the Initial compensation to stabilization, about a week (provided adequate fluid intake and constant Clen dosage. Then after that week or so, it would still be elevated but mainly to the increase in blood volume

[jimmyinkedup]

1)

And with this... Seriously? How f-in childish it this post. You post a snarky post aimed towards me, and I respond to it; then you go and delete what you said then post a response basically making it look like i came out of nowhere with that insult and you are the 'good hearted' person by giving me the 'entitled opinion' bullsh*t? That is freakin childish. Grow up.

You pompous douche bag. I posted and immediately thought you know what ..im gonna take the high road and took it down. This was done before your response as far as i knew. When I saw your response I still refused to lower myself.
This post just shows me it doesn't matter what road you take with you, you arrogant , condescending , ego maniacal prick. Its sad , because if you were more concerned with find out whats truly correct than proving your theories right - you would be an amazing asset.
Stay the fvck away from me marc ......

[Swifto]

And Common trait? Ill take that as a compliment because it was a debate, where i never just gave blatant insults but actually intellectually responded to what I was getting for responses. So, Thanks. I can debate without getting upset ( minus this post, cuz its pathetic), and actually have intelligent responses where i respond to all aspects of the original comment.

Don't ever take anything I've ever said to you as a compliment, nor anything I say in the future. I think your a f*cking doughtnut with half a brain.

Go and prove to the world why the earth is flat because you think it is. Or play in traffic.

You pompous douche bag. I posted and immediately thought you know what ..im gonna take the high road and took it down. This was done before your response as far as i knew. When I saw your response I still refused to lower myself.
This post just shows me it doesn't matter what road you take with you, you arrogant , condescending , ego maniacal prick. Its sad , because if you were more concerned with find out whats truly correct than proving your theories right - you would be an amazing asset.
Stay the fvck away from me marc ......

Makes two of us.

Reminds me of Ross. Has to be right, plays down "minor details" if he's proven wrong and never lets go of it.

[t-dogg]

Great read! Lol...

[Lemonada8]

Well swifto and jimmy, y'all are entitled to your own opinion. And thanks I like doughnuts.
And jimmy how did u delete ur comment before my reply? ESP when I basically was using the same Aspect of what u said? Nice try thi but hey they r both gone so u never know, shoulda quoted what I said.. And u really did lower urself by trying to erase what u said then try to look like the mature one and make me look like the a**. That is what I meant by childish. Congrats

And I refuse when I was "proven" wrong? Noone actually debated with what I was saying (other than Asiandude), all y'all did was repeat I'm wrong, and swifto u never even said anything other than "it's getting old, blah blah blah" and never actually contributed other than to back up who disagreed.
Yall say u want healthy debates and u guys are the ones basically insulting and being hypocritical.
And I disregard the minor details? OoOo beta 1 vs. beta 2 in kidney really kills my whole stance huh? Yea not really, when I KEPT SAYING its a sympathetic response, which would elicit beta 1 activation in the kidney: so that really didn't change much huh.
And ur body doesn't over compensate right? Well if it was "only contractility and hr increase" the blood pressure should still drop (Bp= cardiac output x tpr *total peripheral resistance) and with vasodilation with a chronic supra therapeutic dose of a vasodilator (clen) then the hr and contractility would only get the Bp close to normal but still would be lower, if it went any higher that would be, u guessed it, OVERCOMPENSATION. So the fact that it does kinda throws that argument out of the water that it's purely due to Clens ability to increase contractility and hr. to be actually factually correct beta 2 agonism won't solely increase it that much. It's like what, 4:1 beta1 vs. beta2 receptors in the heart? (and go ahead and search for some article that says differently in the ratios just to disprove me... Still doesn't change the fact that beta 1 far outweighs beta 2 in the heart; wait that's one of those 'minor details' that I disregard because that's exactly what they are, minor details) And yet the arteries have beta 2 throughout? That combined with the efficacy and selectiveness of clen towards beta2, (already shown by the article i posted earlier, which is apparently flawed because it supports my claim... Which by that logic, any study u post I can use the same reply but if I do, then I'm just being stubborn and whatever else adjective u wanna use) the vasodilation would always increase more than the heart effects. (the tpr would keep going down faster than the cardiac output (contractility and hr) could increase). (and I bet the increase in contractility has more to do with Frank-Starling mechanics than activation of a receptor that's not predominately on the heart in the first place.)

How about just accepting the fact that u really only know physio skin deep and when it gets deeper and combines multiple systems, and I even try to include physiologic equations to help support my stance in the topic which, *its a shock I bet* I just didn't make up but is actually legitimate physiology concepts, go ahead and look them up, here's a book u can prolly find free as a chm file to find out for yourself "GUYTON and Hall textbook of medical physiology". u really don't understand and don't care to; so you resort to just screaming along with throwing prolly one of the few physio equations u know to disprove me, and make ZERO sense whatsoever. (and funny thing is, I didn't just insult u about it; I asked what u were tryin to say because it did make no sense... Still waiting on that)
as much ad possible on a forum, that I'm wrong and need to stop and give it up; when there has been basically NO response to the other mechanisms I talked about and how they are being applied incorrectly (minus the bit about how obscure they are... LOL!)

U know it's a real shame when the "role models" on this forum are so short sighted and resort to insults and such instead of actually responding to what is being said: and not letting emotions take over when u really have nothing to say. That is what is really getting old, not the fact that I debate things and try to determine why something is occurring. It's not the fact that "I have to be right" but more of the fact that it ultimately turns into me trying to explain myself and how I am looking at the issue and y'all just keep saying "no" and never responding to what my view is and how it is incorrect. If y'all would do that, then sure I'll admit I'm wrong or had it misconstrued; but since that never happens... Y'all can think wtf u want to cuz u just repeating yourself and throwing insults out there only further increases the viability of my side of the topic because u really don't have any response whatsoever.

[Sworder]

U know it's a real shame when the "role models" on this forum are so short sighted and resort to insults and such instead of actually responding to what is being said: and not letting emotions take over when u really have nothing to say. That is what is really getting old, not the fact that I debate things and try to determine why something is occurring. It's not the fact that "I have to be right" but more of the fact that it ultimately turns into me trying to explain myself and how I am looking at the issue and y'all just keep saying "no" and never responding to what my view is and how it is incorrect. If y'all would do that, then sure I'll admit I'm wrong or had it misconstrued; but since that never happens... Y'all can think wtf u want to cuz u just repeating yourself and throwing insults out there only further increases the viability of my side of the topic because u really don't have any response whatsoever.

I couldn't have worded it better myself. The truth is spoken.

[AD]

My personal view, again not based on research papers, is that the selective vasodilation of coronaries, hepatic, and skeletal muscle vessels, with corresponding vasoconstriction to other vessels, do not change TPR very much(at least not downwards). You said that vasoconstriction of mesenteric vessels are not via beta2, but it should fall within the minor difference you labelled under sympathetic response.

So with TPR unchanged or undecreased, the increase pulse rate and contractility is responsible for the increase in pressure.

This should fall within the timeframe that users of clen normally feel increase in heart beats and BP. Within a few hrs at most. Not 2 to 3 days via water retention.

Lemonada. I appreciate you naming me as trying to argue your points. I also respect you in a way, as you are clearly a student of physiology. But i cannot say the same about your cheerleading team, who at most are a couple of juiceheads who obviously go to google more often than going to school.

[Swifto]

I couldn't have worded it better myself. The truth is spoken.

Sure, because you've been here such a long time haven't you.

[Swifto]

U know it's a real shame when the "role models" on this forum are so short sighted and resort to insults and such instead of actually responding to what is being said: and not letting emotions take over when u really have nothing to say. That is what is really getting old, not the fact that I debate things and try to determine why something is occurring. It's not the fact that "I have to be right" but more of the fact that it ultimately turns into me trying to explain myself and how I am looking at the issue and y'all just keep saying "no" and never responding to what my view is and how it is incorrect. If y'all would do that, then sure I'll admit I'm wrong or had it misconstrued; but since that never happens... Y'all can think wtf u want to cuz u just repeating yourself and throwing insults out there only further increases the viability of my side of the topic because u really don't have any response whatsoever.

Yeah that "never happens" Marc. Like that time you got confused and thought women don't have DHT receptors not too long ago.

Somtimes your f*cking way off.

Other time your wrong and then blame it on "minor details" and "I had it misconstrued". Do you think people on this forum are stupid? You're deluded.

[Lemonada8]

Yeah that "never happens" Marc. Like that time you got confused and thought women don't have DHT receptors not too long ago.
Somtimes your f*cking way off.
Other time your wrong and then blame it on "minor details" and "I had it misconstrued". Do you think people on this forum are stupid? You're deluded.

Not to long ago? that was what 4 years ago when i first started really diving into the whole physiology topic? And pretty sure i didnt argue about that one; all i knew was that DHT is what drives sexual differentiation. And pretty sure i didnt argue about it, and it was a learning experience.

and now to disprove what i have been saying is to say ive been wrong in the past? then with that logic, NOONE EVER would be correct cuz we all make mistakes.


Blame it on minor details and misconstrued huh? yep.. 2 different attitudes there. One is admiting i was wrong ( misconstrued) and the other is still admitting i was wrong but still not fully sold on it ( minor details).

Do you think people on this forum are stupid? u act like u know everything and if someone challanges your so-called knowledge, u turn into a egotistical male donkey and just want to insult n such without actually saying anything.

[Lemonada8]

My personal view, again not based on research papers, is that the selective vasodilation of coronaries, hepatic, and skeletal muscle vessels, with corresponding vasoconstriction to other vessels, do not change TPR very much(at least not downwards). You said that vasoconstriction of mesenteric vessels are not via beta2, but it should fall within the minor difference you labelled under sympathetic response.
So with TPR unchanged or undecreased, the increase pulse rate and contractility is responsible for the increase in pressure.
This should fall within the timeframe that users of clen normally feel increase in heart beats and BP. Within a few hrs at most. Not 2 to 3 days via water retention.
Lemonada. I appreciate you naming me as trying to argue your points. I also respect you in a way, as you are clearly a student of physiology. But i cannot say the same about your cheerleading team, who at most are a couple of juiceheads who obviously go to google more often than going to school.

Ok, i think i see where you are coming from now.
Clen will only elicit a partial sympathetic response (via beta 2 receptors) which is primarily vasodilation in the arterioles. Arterioles are the main place for TPR ( total peripheral resistance) regulation and control flow to the capillaries. These receptors differ in density depending on what the tissue is; Arteries going to Muscle for instance, has lots of B2 receptors to increase the blood flow to the muscles when needed; The arteries leading to the Gut are primarily lined with Alpha 1 receptors (which will vasoconstrict) when needed, yet there are still some beta 2 receptors in the Gut which will vasodilate.
When the sympathetic system is activated, both alphas and betas are 'hit'; which result in the typical effects of the sympathetic response of increased blood flow to the muscles and decreased flow to the gut and increased HR and contractility.
However, when only a selective receptor is hit; the other sympathetic effects dont occur via that drug. So in this case, clen is a beta 2 agonist which will vasodilate the arterioles. This dilation decreases the resisitance drastically very similar to how you get increased blood flow to the muscles with exercise (but the body doesnt secrete beta2 selective activators, so the other receptors will be 'hit'). Also, with resistance; it follows Poiseuille’s law ( basically saying that Resistance=1/Radius^4) so any minor change in the radius size of the arteriole has a drastic change in resistance, that combined with the opening of capillary beds (in parallel fashion) will result in a large drop in resistance.
The corresponding vasoconstriction will not occur by clens actions at all, being that vasoconstriction occurs via Alpha1.

The increase in BP and HR is due to a sympathetic response to the immediate drop in TPR ( which is sensed as a drop in perfusion, so the body responds). that is what causes the inital increase in BP, then chronically the increased BP is due to the increased fluid retention ( because of the increased area for the blood to go). The body cant stay in a constant state of sympatetic response to the decrease in perfusion, which is where the fluid retention comes in to increase the circulating blood volume. This is also shown to be accurate due to the massive urination following clen use ( the excess fluid isnt needed anymore because the chronic vasodilation has stopped, decreasing the area for blood to go, increasing the TPR; which is then excreted by the kidneys)
There is also the constriction of veins (alpha1) which increases the circulating blood volume ( ~70% is just chillin in the veins) initially to help cover the fluid needs acutely: another part of the sympathetic response.
Then there is the bit about the 2nd messanger system i said earlier, about how Alpha1 and Beta2 send their message in the cell; well with a higher number of beta2 receptors in the muscle ( which can hold ALOT of blood), the vasodilation is more pronounced there. In the mesenteric arteries where alpha1 predominates, the sympathetic effect on Alpha1 will vasoconstrict those arteries much more than they were ever dilated with Clen hitting Beta2.
The attempt of vasoconstriction done by the sympathetics in the muscles is much more futile (with beta2 being predominate over alpha1).

Does that make more sense?

[Sworder]

Yeah that "never happens" Marc. Like that time you got confused and thought women don't have DHT receptors not too long ago.
Somtimes your f*cking way off.
Other time your wrong and then blame it on "minor details" and "I had it misconstrued". Do you think people on this forum are stupid? You're deluded.

Nobody has DHT receptors, DHT binds to the androgen receptor and then it has DHT specific DNA sequences which promote DHT-AR complex gene expressions. We have 5 alpha reductase enzymes which convert T to DHT if that is what you are talking about. I don't mean to be nitpicking but it just sounds very funny to hear "DHT receptor". I am sure that you are referring to 5AR enzymes which are predominantly present in androgen specific tissue such as the prostate, skin and causes MPB due to high concentration of 5AR in the scalp.

I may be wrong, but I highly doubt it.

[Bonaparte]

Nobody has DHT receptors, DHT binds to the androgen receptor and then it has DHT specific DNA sequences which promote DHT-AR complex gene expressions. We have 5 alpha reductase enzymes which convert T to DHT if that is what you are talking about. I don't mean to be nitpicking but it just sounds very funny to hear "DHT receptor". I am sure that you are referring to 5AR enzymes which are predominantly present in androgen specific tissue such as the prostate, skin and causes MPB due to high concentration of 5AR in the scalp.

I may be wrong, but I highly doubt it.

No, we had a big debate about this some while back, pubmed was ransacked, and specific DHT receptors were found. lol
I hadn't heard of them either until then (they aren't very abundant and mostly located in genitalia, if I recall).

[Sworder]

No, we had a big debate about this some while back, pubmed was ransacked, and specific DHT receptors were found. lol
I hadn't heard of them either until then (they aren't very abundant and mostly located in genitalia, if I recall).

Mind boggling, do you recall the name of the thread?

[Bonaparte]

Mind boggling, do you recall the name of the thread?

I'm trying to look for it right now.
Now that I'm thinking harder, it started off as a question about women using Winstrol. Lemonada said that winstrol wouldn't work well for women because they lack DHT receptors. I pointed out that they have androgen receptors, which are activated by DHT and its analogues (and added that there is no such thing as a DHT-specific receptor). He conceded that that made sense, but then dug up pubmed studies referencing a DHT receptor in males that plays a large part in erections, but IDK if we ever settled on that being another term for an androgen receptor, or if it something different.

[Sworder]

I would think it just refers to the DHT-(androgen)receptor complex. I would be interested in finding something that refers to it, I browsed all your posts and Lemonades a quicky...

[AD]

Ok, i think i see where you are coming from now.
Clen will only elicit a partial sympathetic response (via beta 2 receptors) which is primarily vasodilation in the arterioles. Arterioles are the main place for TPR ( total peripheral resistance) regulation and control flow to the capillaries. These receptors differ in density depending on what the tissue is; Arteries going to Muscle for instance, has lots of B2 receptors to increase the blood flow to the muscles when needed; The arteries leading to the Gut are primarily lined with Alpha 1 receptors (which will vasoconstrict) when needed, yet there are still some beta 2 receptors in the Gut which will vasodilate.
When the sympathetic system is activated, both alphas and betas are 'hit'; which result in the typical effects of the sympathetic response of increased blood flow to the muscles and decreased flow to the gut and increased HR and contractility.
However, when only a selective receptor is hit; the other sympathetic effects dont occur via that drug. So in this case, clen is a beta 2 agonist which will vasodilate the arterioles. This dilation decreases the resisitance drastically very similar to how you get increased blood flow to the muscles with exercise (but the body doesnt secrete beta2 selective activators, so the other receptors will be 'hit'). Also, with resistance; it follows Poiseuille’s law ( basically saying that Resistance=1/Radius^4) so any minor change in the radius size of the arteriole has a drastic change in resistance, that combined with the opening of capillary beds (in parallel fashion) will result in a large drop in resistance.
The corresponding vasoconstriction will not occur by clens actions at all, being that vasoconstriction occurs via Alpha1.

The increase in BP and HR is due to a sympathetic response to the immediate drop in TPR ( which is sensed as a drop in perfusion, so the body responds). that is what causes the inital increase in BP, then chronically the increased BP is due to the increased fluid retention ( because of the increased area for the blood to go). The body cant stay in a constant state of sympatetic response to the decrease in perfusion, which is where the fluid retention comes in to increase the circulating blood volume. This is also shown to be accurate due to the massive urination following clen use ( the excess fluid isnt needed anymore because the chronic vasodilation has stopped, decreasing the area for blood to go, increasing the TPR; which is then excreted by the kidneys)
There is also the constriction of veins (alpha1) which increases the circulating blood volume ( ~70% is just chillin in the veins) initially to help cover the fluid needs acutely: another part of the sympathetic response.
Then there is the bit about the 2nd messanger system i said earlier, about how Alpha1 and Beta2 send their message in the cell; well with a higher number of beta2 receptors in the muscle ( which can hold ALOT of blood), the vasodilation is more pronounced there. In the mesenteric arteries where alpha1 predominates, the sympathetic effect on Alpha1 will vasoconstrict those arteries much more than they were ever dilated with Clen hitting Beta2.
The attempt of vasoconstriction done by the sympathetics in the muscles is much more futile (with beta2 being predominate over alpha1).

Does that make more sense?

there, thats how my vasoconstriction takes place.

[jimmyinkedup]

Yeah that "never happens" Marc. Like that time you got confused and thought women don't have DHT receptors not too long ago.

Somtimes your f*cking way off.

Other time your wrong and then blame it on "minor details" and "I had it misconstrued". Do you think people on this forum are stupid? You're deluded.

i do remember ....within the last year...then revisited in the OTHER clen less time ago than that.

[m1k333]

I have just bough 100 clen 20 tablets, it will be my first time taking this, how much mg should I take per day?

[mrglorious]

I have just bough 100 clen 20 tablets, it will be my first time taking this, how much mg should I take per day?

Start with 40mg. Work ur way up to 100mg then taper down to 40mg. 2weeks cycle.

Pain is weakness leaving the body!

[evander87]

Start with 40mg. Work ur way up to 100mg then taper down to 40mg. 2weeks cycle.

Pain is weakness leaving the body!

Don't taper it's a waste of the compound.

Slowly work your way up to max dosage (120-160) after 14days just stop and wait two more weeks to hit it again.

BTW I've had better results at 120 than I did at 160. At 160 my workouts sucked and fat loss was minimal do to crappy workouts.

[m1k333]

Okay thanks a lot for the advice, ill give it a bash!