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Beta Blockers potentiate stimulants?

SpunkySkunk347

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I have heard from multiple sources that beta blockers (epinephrine antagonists) will potentiate stimulants (particularily ones where NE stimulation is an unwanted side effect)

They leave the stimulant high as a much more relaxing dopaminergic/serotonergic euphoria, and less of a tweaking insomnia high.
Could anyone with a little more knowledge of neurochemistry explain exactly why beta blockers potentiate stimulants?
 
Mixing beta blockers with stimulants (except perhaps with low doses of both) is dangerous, and contraindicated medically. Blocking action at the beta-adrenergic receptors leads to increased action at the alpha-adrenergic receptors, with potentially life threatening consequences.

I've explained the mechanism of why beta blockers are problematic in more detail here:

Alpha-blockers would likely be more effective at lowering heart rate because they reduce peripheral constriction. Heart rate is proportional to peripheral vascular resistance (the heart has to work harder to circulate blood to peripheral tissue when its vasoconstricted). For this reason alpha1/alpha2 antagonists are used to treat amphetamine ODs, and beta blockers are not.


SpunkySkunk347 said:
I have heard from multiple sources that beta blockers (epinephrine antagonists) will potentiate stimulants (particularily ones where NE stimulation is an unwanted side effect)

They leave the stimulant high as a much more relaxing dopaminergic/serotonergic euphoria, and less of a tweaking insomnia high.
Could anyone with a little more knowledge of neurochemistry explain exactly why beta blockers potentiate stimulants?
 
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Hmmm... I'm not convinced. Yeah, I can see the logic if we had a selective B2 receptor antagonist. But if we were talking about metoprolol/atenolol I'd find it hard to believe this would cause an increase in BP and HR.

You got any evidence to convince me (apart from what ER docs do, because really, they're not know for their evidence based approach).
 
ou know BilZ0r, its funny, I've found this bit of information paraphrased in a number of my emergency medicine textbooks, yet none ever cite any references for it. Even in the primary literature, I see it stated without citations.

For example, this article is a comprehensive up to date review on amphetamine/MDMA toxicity and ER management. It goes through each organ system, listing the toxic effects specific to that system and the appropriate medical management to counteract it. Yet the one paragraph that talks about the preferential use of alpha blockers over beta blockers has no citations!

I'll quote the paragraph either way, just in case it helps to increase the understanding of others on this issue. Based on my own understanding of medical physiology, the explanation makes sense... but I do agree it would be nice to have some case reports at least to back this up.

SR White. 2002. Amphetamine toxicity. Semin Respir Crit Care Med. 23(1):27-36. said:
ß-blocking agents should be avoided because unopposed a-receptor-mediated vasoconstriction could result in increased blood pressure or coronary artery vasoconstriction. The combined a and ß-receptor blocking effects of labetalol would seemingly make it a logical choice except that the a-blocking effects are relatively weak. Hypertension could be managed with an a-receptor blocking agent such as phentolamine or with direct-acting vasodilators such as nitrates, hydralazine, or nitroprusside.

I should also just clarify that any increased HR would be reflexive in response to sudden increased peripheral vasoconstriction as the heart needs to work harder to overcome the additional afterload. Administering a beta-blocker would not cause an increase in HR through any direct mechanism.


BilZ0r said:
Hmmm... I'm not convinced. Yeah, I can see the logic if we had a selective B2 receptor antagonist. But if we were talking about metoprolol/atenolol I'd find it hard to believe this would cause an increase in BP and HR.

You got any evidence to convince me (apart from what ER docs do, because really, they're not know for their evidence based approach).
 
Limpet_Chicken said:
Wouldn't A2 agonists do better than antagonists? they lower blood pressure quite effectively.

True. Agonism at A2 does cause vasodilation and lowers BP, BUT, agonism at either A1 or A2 has the nasty side effect of vasoconstricting the coronary arteries. This on a background of amphetamine use is a recipe for myocardial infarction. Selective A1 antagonists are preferred for this reason.
 
Alpha-2 adrenoreceptors are the way negative feedback is exerted on the sympatheyic nervous system, so in the presence of a stimulant like amphetamine I'd think it'd be a bit dodgy using an alpha-2 agonist as it could lead to postural hypotension (you stand up, you black out, you wake up pissing blood from a would from keeling over in an uncontrolled manner)

Basically, I'd avoid any of the adrenergic blockers if taking a stimulant unless something like a hypertensive crisis was immenant; then I'd want it done in an A&E/ER enviroment in case things went horribly wrong - it's not the sort of thing to be attempted as a home remedy as things like that or hyperthermia (I've read posts asking about treating hyperthermia at home using dantrolene - a very bad idea as malignant hyperthermia is a definite indicator for ambulances & ITU treatment in almost all cases) unless you have a death wish.

And they're pretty fuckin' horrible ways to kick the bucket - the sort of thing that involves lots of screaming & suffering. If in doubt, take nowt (just ring for help a.s.a.p. - no excuses otherwise)
 
Speaking from a purely ancedotal perspective, i've been taking atenolol and low to moderate doses of dexedrine. I usually never get beyond 50mg in a 24 hour period though which is laughable compared to serious D-AMP users im sure.

While i've definetly heard the theory that taking a beta blocker while under the influence of an amphetamine is not wise and causes a possible hypertensive crisis via alpha receptors im not aware or unclear on any actual interaction between the two substances thats been documented. Rather the warning is not to administer a beta blocker to someone who is allready hypertensive because of amphetamine.
 
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