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Vasodilators?


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#1 bgwithadd

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Posted 29 December 2008 - 11:20 PM


The problem with stims is the vasoconstriction. I have been unhappy with this side effect a while and was wondering if it was possible to safely counteract it, hopefully with something that's not prescription. If it's something that doesn't last 24 hours that might be better because I only want it to counteract the effects of stims.

#2 graatch

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Posted 04 January 2009 - 03:03 PM

The problem with stims is the vasoconstriction. I have been unhappy with this side effect a while and was wondering if it was possible to safely counteract it, hopefully with something that's not prescription. If it's something that doesn't last 24 hours that might be better because I only want it to counteract the effects of stims.


Just what immediately comes to mind -- pomegranate extract (standardized for punicalagins) or juice, reishi mushroom, horsechestnut extract, pine bark or grape seed extracts, all have hard data supporting a lasting effect of lowered blood pressure. Pomegranate in particular is reputed for this purpose, seeming as it does to work by a few different mechanisms for acute lowering of BP, improve the health of the arterial walls over time, and measureably lower markers of systemic inflammation and oxidative stress.

I do take BAC's pomegranate p40p powder, and ginkgo biloba (which lowers BP not by vasodilation but reducing viscosity) with my dextroamphetamine ... my blood pressure last tested at 108/72, so I'm happy. Actually, it's definitely the case for me that, in many situations, my blood pressure is noticeably lower WITH d-amp than it would be without, I think because I do not become as stressed or overwhelmed doing simple things ... but these supplements do noticeably keep down a general resting elevation that the drug can sometimes provoke.

This is by no means a complete explanation of these agents, check them out. Lots of threads here and resources elsewhere.

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#3 bgwithadd

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Posted 04 January 2009 - 11:42 PM

Thanks for the info, I didn't know a lot of these. I had forgotten about this. The pine bark seems to help, I think I will get some in bulk so it's affordable.

My bp does ok but the problem is that I am getting obvious problems from the vasoconstriction. My skin is not as good and embarassingly I seem to have trouble keeping a strong erection now that I've been using stims a while. Actually, I think the nicotine was the biggest offender and I have dropped it from my daily lineup for now and I seem much better, but I'd like to avoid these issues entirely.... Would be great if I found something to actually make me able to use the patchs again as they work really well, but if I can't I can't.
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#4 Guacamolium

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Posted 04 January 2009 - 11:59 PM

Caffeine non-selectively inhibits phosphodiesterase enzymes 1-5, and vinpocetine selectively inhibits phosphodiesterase 1 which will help with vasodilation. You can always try citrulline malate, L-arginine, arginine ethyl ester, etc as they cause increased nitric oxide presence in the blood. Short-lived though, so try for extended release of those if you can. Pentoxifylline is an option as well.

#5 NDM

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Posted 05 January 2009 - 01:06 AM

Can one clarify for me the relation between mental performance, vasoconstriction, and vasodilation? In the state of ignorance I am in, I am tempted to reason along these lines:

If stimulants like caffeine and nicotine increase mental performance by means of vasoconstriction, wouldn't it follow that vasodilators like vinpo and ginkgo lower mental performance?

Or is vasoconstriction a mere side effect of stimulants, unrelated to the mechanism by which they affect mental performance?

If the former line of reasoning holds true, a pragmatic move would be to relegate all vasodilators to times when one does not need to be in peak mental shape (e.g. sleep)

Thanks in advance
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#6 bgwithadd

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Posted 05 January 2009 - 02:00 AM

Thanks, carson. More good ideas to try.

@ndn - the vasoconstriction is just a side effect of most stims. The stims help by working on the dopamine and ne receptors and possibly the dopamine transporters to help speed up the prefrontal cortex and stimulate reward centers. The nicotine seemed especially strong in regard to vasoconstriction or else I am especially sensitive to its effects.
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#7 medicineman

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Posted 05 January 2009 - 09:07 AM

the relationship is the fact that dopamine and monoamines (which are the target of stimulants and caffeine) exert a constrictor effect on vessels, and they are the same chemicals which give you the edge in thinking. so, you have a double edged sword.

caffeine also blocks adenosine. Here is something nice to know about why caffeine keeps you up.


Adenosine in sleep and wakefulness
by
Porkka-Heiskanen T
Institute of Biomedicine, University of Helsinki, Finland.
Ann Med 1999 Apr; 31(2):125-9

ABSTRACT

Sleep propensity increases in the course of wakefulness: the longer the previous wakefulness period is, the longer and deeper (measured as delta power in EEG recordings) is the following sleep. The mechanisms that regulate the need of sleep at the cellular level are largely unknown. The inhibitory neuromodulator, adenosine, is a promising candidate for a sleep-inducing factor: its concentration is higher during wakefulness than during sleep, it accumulates in the brain during prolonged wakefulness, and local perfusions as well as systemic administration of adenosine and its agonists induce sleep and decrease wakefulness. Adenosine receptor antagonists, caffeine and theophylline, are widely used as stimulants of the central nervous system to induce vigilance and increase the time spent awake. Our hypothesis is that adenosine accumulates in the extracellular space of the basal forebrain during wakefulness, increasing the sleep propensity. The increase in extracellular adenosine concentration decreases the activity of the wakefulness-promoting cell groups, especially the cholinergic cells in the basal forebrain. When the activity of the wakefulness-active cells decreases sufficiently sleep is initiated. During sleep the extracellular adenosine concentrations decrease, and thus the inhibition of the wakefulness-active cells also decreases allowing the initiation of a new wakefulness period.



#8 navyblue

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Posted 26 January 2009 - 08:44 AM

Could someone please explain to me why a vasodialator that does not have any stimulating effects such as l-arginine will knock someone out (making them extremely tired)?

#9 Guacamolium

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Posted 26 January 2009 - 01:57 PM

Could someone please explain to me why a vasodialator that does not have any stimulating effects such as l-arginine will knock someone out (making them extremely tired)?


Its function of a vasodilator is fairly potent and very short-lived. Due to this, blood pressure will drop fast, possibly causing the symptoms you are experiencing - considering that you aren't taking anything else with arginine that is exacerbating that effect further. Perhaps try citrulline malate - the precursor to arginine.

#10 navyblue

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Posted 26 January 2009 - 04:02 PM

I see, so its only after the drug wears off (meaning the blood vessels are now contracting) that the blood pressure drops?

I originally thought it was the dilation of the blood vessels that caused the blood pressure to drop and not the constriction?

#11 nowayout

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Posted 26 January 2009 - 04:42 PM

I see, so its only after the drug wears off (meaning the blood vessels are now contracting) that the blood pressure drops?


No.

I originally thought it was the dilation of the blood vessels that caused the blood pressure to drop and not the constriction?


You thought right.

#12 navyblue

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Posted 26 January 2009 - 05:36 PM

I'll try to pick up some citrulline malate within the week. What are the other long acting vasodilators out there besides caffeine and the nicotine patch, if any?

I ask because Excedrin (tension headache formula) which contains (65mg of caffeine) helps my tension headaches really well. I of course attribute this to the vasodilation of blood vessels.

Ashwagandha, l-tyrosine, adderall, and other stimulants seem to cause vasoconstriction (which i attribute to the tension headaches), at least for me. So about 1 hour ago I decided to take some Ashwagandha with Excedrin to see if the caffeine would eliminate the tension headache cause by the ashwagandha. So, far so good, no tension headaches as of yet, unfortunately I am starting to get a bit of pressure in my ears (an ongoing problem for me when taking stimulants). My ears tend to pop really easily. I don't want too stray to far off topic,

Okay so here is another question (sorry didn't mean to put you guys on jeopardy). When you go up in a plane, or high up a mountain, etc and your ears pop, does that have anything to do with vasodilation or vasoconstriction?

I guess what I am asking is, what causes our ears to pop? After taking certain drugs (stimulants mainly), my ears tend to pop (constant feeling of pressure), but I cannot seem to relieve it.

#13 revnik

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Posted 26 January 2009 - 07:42 PM

I'll try to pick up some citrulline malate within the week. What are the other long acting vasodilators out there besides caffeine and the nicotine patch, if any?


Caffeine&nicotine are vasocontrictors :)
Vinpocetine, Ginkgo, ... are vasodilators.

#14 bgwithadd

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Posted 02 February 2009 - 08:13 AM

I don't think gingko is a vasodilator, and vinpocitine is neural selective.

Anyway, I tried a few things but I settled on forskolin. It doesn't work through NO, and I suspect that too much NO is not a great idea so that's why I chose it. It seems to be surprisingly effective.

#15 Guacamolium

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Posted 02 February 2009 - 05:23 PM

I don't think gingko is a vasodilator, and vinpocitine is neural selective.

Anyway, I tried a few things but I settled on forskolin. It doesn't work through NO, and I suspect that too much NO is not a great idea so that's why I chose it. It seems to be surprisingly effective.


I have forskolin. What mechanism does it vasodilate through? I wasn't even aware that it's a candidate for vasodilation...

#16 Guacamolium

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Posted 02 February 2009 - 05:25 PM

I don't think gingko is a vasodilator, and vinpocitine is neural selective.

Anyway, I tried a few things but I settled on forskolin. It doesn't work through NO, and I suspect that too much NO is not a great idea so that's why I chose it. It seems to be surprisingly effective.


I have forskolin. What mechanism does it vasodilate through? I wasn't even aware that it's a candidate for vasodilation...



#17 bgwithadd

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Posted 02 February 2009 - 09:24 PM

It increases cAMP, and one of the things that ultimately does downstream is vasodilation by relaxing muscle. From some paper online "Forskolin and milrinone both increase cyclic AMP concentrations to enhance cardiac contractility and cause vascular dilation in vitro and in vivo".

I didn't expect it to work well, but it works very well. Heartbeat slows, bp drops, and I can feel my veins are very soft and more visible...and more than anything, I don't get so incredibly cold any more in my hands feet etc. when I am on adderal.

For normal person I think 1-2 125mg pills would be plenty but since I take vasoconstrictors like crazy I am taking two every time I have any addy, and one when I eat lunch and oen when I go to bed.

#18 HenryHH

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Posted 02 February 2009 - 10:19 PM

How about L-Arginine AKG?

#19 bgwithadd

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Posted 02 February 2009 - 11:50 PM

The problem is that it doesn't last long and since it uses NO you get tolerance pretty quick (seemingly due to it actually causing damage). It might be ok and I might try it, but I'd rather look for other mechanisms - and forskolin seems to be pretty good in this respect. I'd really like to find a strong PDE4 inhibitor, though.

#20 nowayout

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Posted 03 February 2009 - 01:39 PM

The problem is that it doesn't last long and since it uses NO you get tolerance pretty quick (seemingly due to it actually causing damage). It might be ok and I might try it, but I'd rather look for other mechanisms - and forskolin seems to be pretty good in this respect. I'd really like to find a strong PDE4 inhibitor, though.


Yes, while short-term studies of arginine often show benefit, long-term administration of arginine can be harmful because of tolerance. The following paper showed that over 6 months, arginine was significantly worse than placebo for PAD. You can find the entire paper for free if you google it. The graphs are pretty frightening.


L-Arginine Supplementation in Peripheral Arterial Disease

No Benefit and Possible Harm
Andrew M. Wilson, MBBS, PhD; Randall Harada, MD; Nandini Nair, MD, PhD; Naras Balasubramanian, PhD; John P. Cooke, MD, PhD From the Division of Cardiovascular Medicine (A.M.W., R.H., N.N., J.P.C.) and Department of Biostatistics (N.B.), Stanford University School of Medicine, Stanford, Calif.

Correspondence to John P. Cooke, MD, PhD, Division of Cardiovascular Medicine, Stanford University Medical Center, Falk Cardiovascular Research Institute, 300 Pasteur Dr, Stanford, CA 94305. E-mail john.cooke@stanford.edu

Received December 20, 2006; accepted May 3, 2007.

Background— L-Arginine is the precursor of endothelium-derived nitric oxide, an endogenous vasodilator. L-Arginine supplementation improves vascular reactivity and functional capacity in peripheral arterial disease (PAD) in small, short-term studies. We aimed to determine the effects of long-term administration of L-arginine on vascular reactivity and functional capacity in patients with PAD.

Methods and Results— The Nitric Oxide in Peripheral Arterial Insufficiency (NO-PAIN) study was a randomized clinical trial of oral L-arginine (3 g/d) versus placebo for 6 months in 133 subjects with intermittent claudication due to PAD in a single-center setting. The primary end point was the change at 6 months in the absolute claudication distance as assessed by the Skinner-Gardner treadmill protocol. L-Arginine supplementation significantly increased plasma L-arginine levels. However, measures of nitric oxide availability (including flow-mediated vasodilation, vascular compliance, plasma and urinary nitrogen oxides, and plasma citrulline formation) were reduced or not improved compared with placebo. Although absolute claudication distance improved in both L-arginine- and placebo-treated patients, the improvement in the L-arginine-treated group was significantly less than that in the placebo group (28.3% versus 11.5%; P=0.024).

Conclusions— In patients with PAD, long-term administration of L-arginine does not increase nitric oxide synthesis or improve vascular reactivity. Furthermore, the expected placebo effect observed in studies of functional capacity was attenuated in the L-arginine-treated group. As opposed to its short-term administration, long-term administration of L-arginine is not useful in patients with intermittent claudication and PAD.



#21 nowayout

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Posted 03 February 2009 - 01:41 PM

The problem is that it doesn't last long and since it uses NO you get tolerance pretty quick (seemingly due to it actually causing damage). It might be ok and I might try it, but I'd rather look for other mechanisms - and forskolin seems to be pretty good in this respect. I'd really like to find a strong PDE4 inhibitor, though.


Have you tried any of the PDE-5 inhibitors?

#22 navyblue

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Posted 03 February 2009 - 03:27 PM

Doesn't forskolin increase thyroid function? Not sure if this is a good thing for long term use.

#23 bgwithadd

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Posted 03 February 2009 - 11:15 PM

andre - I have. They have some great effects, but you don't want to go too crazy with those, either.

navyblue - it can, but that is usually a good thing.



Anyone know if forskolin crosses the BBB? New research shows that cAMP concentrations in the brain are bad for the prefrontal cortex.

#24 Lufega

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Posted 27 February 2009 - 06:35 AM

Anyone know if forskolin crosses the BBB? New research shows that cAMP concentrations in the brain are bad for the prefrontal cortex.


Forskolin is small and fat soluble so I speculate that it probably crosses the BBB.

I should get a Darwin award for this. I've been feeling utterly exhausted lately. I have low blood pressure. The last month, I raised the dose of forskolin from 10 mg to 40, each morning fasted. Duh.. ;)

#25 bgwithadd

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Posted 27 February 2009 - 08:27 AM

I tried it a while, too. It is a pretty interesting supplement. I suppose some of the research posted in the other thread shows it crosses the BBB, too. Interestingly, forskolin is also found to tighten the BBB, though.

#26 bgwithadd

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Posted 27 February 2009 - 08:32 AM

Damn, caffeine raises cAMP, as well.

Also, same with sugar/glucose. Or anything that raises blood glucose levels.

The US has the highest sugar, highest caffeine diet in the world, and also the very highest ADD rates. I have to wonder how much of it could be simply due to built up cAMP shutting down the brain.

Another effect of cAMP in the brain looks to be decreases response to GABA, making you much more nervous, causing social anxiety, etc.

Maybe I can find a supplement that works in the opposite way of caffeine and/or forskolin....

Edited by bgwithadd, 27 February 2009 - 08:45 AM.


#27 Lufega

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Posted 27 February 2009 - 05:58 PM

The US has the highest sugar, highest caffeine diet in the world, and also the very highest ADD rates. I have to wonder how much of it could be simply due to built up cAMP shutting down the brain.


Good point. Most people start drinking coffee at an early age mostly as a learned behavior. Maybe the increase in brain cAMP over a long period of time does contribute to the levels of ADD rates.

Caffeine inhibits phosphodyesterase, the enzyme that breaks apart cAMP so levels remain high. I don't drink coffee, ever. But the other day, someone gave me a caffeine pill (200 mg?) since I was falling asleep in class. Now that I think about it, I was also on 40 mg forskolin that morning. I got a double whammy. FSK increases cAMP and caffeine prevents it's breakdown. I remember I got an awsome nootropic effect from it.

Another effect of cAMP in the brain looks to be decreases response to GABA, making you much more nervous, causing social anxiety, etc.

Maybe I can find a supplement that works in the opposite way of caffeine and/or forskolin....


Lithium orotate seems to be the only supp. that's been tested head to head with FSK.

I don't want to stop FSK. I switched to taking it at night. During the day, my cognitive functions were a little better and it actually made me tired at night but still left me somewhat stimulated.

Edited by Lufega, 27 February 2009 - 06:01 PM.


#28 Duke

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Posted 28 February 2009 - 12:12 AM

http://www.scienceda...70420143324.htm

Raises questions as to the efficacy of guanfacine as a nootropic.

Caffeine, however, shown to undermine hippocampus-dependent learning and memory tasks (also undermining hippocampal neurogenesis) with long term use - along with its pro cAMP properties - astounds me considering how ubiquitous it is. More reason to cycle caffeine and enjoy the quasi-amphetamine effects vs. being addicted and eventually requiring caffeine just to preform as well as one could without it to begin with. How very insidious this otherwise apparently useful drug is.

Adenosine in sleep and wakefulness
by
Porkka-Heiskanen T
Institute of Biomedicine, University of Helsinki, Finland.
Ann Med 1999 Apr; 31(2):125-9

ABSTRACT

Sleep propensity increases in the course of wakefulness: the longer the previous wakefulness period is, the longer and deeper (measured as delta power in EEG recordings) is the following sleep. The mechanisms that regulate the need of sleep at the cellular level are largely unknown. The inhibitory neuromodulator, adenosine, is a promising candidate for a sleep-inducing factor: its concentration is higher during wakefulness than during sleep, it accumulates in the brain during prolonged wakefulness, and local perfusions as well as systemic administration of adenosine and its agonists induce sleep and decrease wakefulness. Adenosine receptor antagonists, caffeine and theophylline, are widely used as stimulants of the central nervous system to induce vigilance and increase the time spent awake. Our hypothesis is that adenosine accumulates in the extracellular space of the basal forebrain during wakefulness, increasing the sleep propensity. The increase in extracellular adenosine concentration decreases the activity of the wakefulness-promoting cell groups, especially the cholinergic cells in the basal forebrain. When the activity of the wakefulness-active cells decreases sufficiently sleep is initiated. During sleep the extracellular adenosine concentrations decrease, and thus the inhibition of the wakefulness-active cells also decreases allowing the initiation of a new wakefulness period.


Explains why fatigue kicks me in the rear end with a complete seven hours of sleep the night before when the night before that I only slept three hours!

Edited by Duke, 28 February 2009 - 12:24 AM.


#29 bgwithadd

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Posted 28 February 2009 - 12:19 AM

I don't notice anything directly with the guanfacine, but I do notice I am using less adderall lately so maybe it does help a bit. I had to step down to just half a mg a day because it was giving me anxiety.

As for caffeine, I wish I knew how bad it was regarding the cAMP production. I mean should it just never be taken? Or is it ok if I have one soda per day which is around 60mg.

Edited by bgwithadd, 28 February 2009 - 12:20 AM.


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#30 Duke

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Posted 28 February 2009 - 12:33 AM

I don't notice anything directly with the guanfacine, but I do notice I am using less adderall lately so maybe it does help a bit. I had to step down to just half a mg a day because it was giving me anxiety.

As for caffeine, I wish I knew how bad it was regarding the cAMP production. I mean should it just never be taken? Or is it ok if I have one soda per day which is around 60mg.


This is all from Wiki:

"An array of studies found that caffeine could have nootropic effects, inducing certain changes in memory and learning. However, the tests performed contradict one another and the results have proven inconsistent and inconclusive."

"In another study, caffeine was added to rat neurons
in vitro. The dendritic spines (a part of the brain cell used in forming connections between neurons) taken from the hippocampus (a part of the brain associated with memory) grew by 33% and new spines formed. After an hour or two, however, these cells returned to their original shape."

"Researchers have found that long-term consumption of low dose caffeine slowed hippocampus-dependent learning and impaired long-term memory in mice. Caffeine consumption for 4 weeks also significantly reduced hippocampal neurogenesis compared to controls during the experiment. The conclusion was that long-term consumption of caffeine could inhibit hippocampus-dependent learning and memory partially through inhibition of hippocampal neurogenesis."

The contradictions stated in the first quote seem almost nauseatingly obvious: short term effects = good, long term effects = bad! I understand that is a blanket statement but the contradictions vs. my simple explanation are irrelevant: the benefits and risks are quite clear.

The last quote partially answers your question. As if daily liquid candy is truly necessary anyway.

Edited by Duke, 28 February 2009 - 12:36 AM.





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