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Alpha & Beta Receptors Discussion

18 posts in this topic

Posted · Report post

Could we have a discussion on alpha-1, alpha-2, beta-1, beta-2 receptors? I have a brief limited understanding of them...but don't really understand how they're connected and integrated completely.

It seems that a receptor can do two things that usually don't go together in the same sympathetic or parasympathetic categories (like one from each category?) and only to specific areas like lungs/heart...it gets confusing.

It would specifically help, in relation to medications, neurotransmitters, physiological systems/processes (like responses to changes in BP), etc... (I'd rather not start off, b/c I'll confuse myself...) 1...2...3...go

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Posted · Report post

Anthony give us a little more info such as...

What drugs do you give that affect A&B (Epi, Salbutomol, etc) that would help guide the discussion.

Ok others may disagree but The 3 most important to BLS are A1, B1, B2,

All 3 are Adrenergic receptor sites. That is to say they are the moderator between the nervous system and the affected organ(s). So....

Beta-1 affected organ is the heart. When stimulated by adrenergic agonists such as Norepinephrine, Epinephrine (whether natural from the adrenal gland or injected by an epipen), it causes the heart to speed up (positive chronotropic), Velocity of conduction is increased (positive dromotropic), And causes an increase in contractile force ( positive inotropy). These positive affects are stimulated by the sympathetic nervous system.

If this is the kind of answer you are lookig for let us know and we will continue...But I am a slow typer to write out all the others if this is not sufficient.

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Posted · Report post

Yeah, that's the exactly the kind of thing I'm talking about. I don't have any specific meds in mine...maybe common ones used in the prehospital setting or commonly prescribed ones, so when I see a patient who has them, I have something to associate it with... I wouldn't be making decisions based on this really...it's just for the info.

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Posted · Report post

Beta 2 has a few actions, the most important to an EMT is Smooth muscle relaxation in the bronchi. Therefore when stimulated by agonists it causes the bronchi to dilate.

Alpha 1 & 2 basically cause vasoconstriction (A-1) and decrease motility in the GI system (A-2).

The parasymathetic nervous system is in charge of autoregulation at rest (feed or breed). The Parasymathetic system uses Acetycholine as a neurotransmitter.

When stimulated by pain, strong emotion, etc, the sympathetic nervous system takes over and you see these affector organs respond (fight of flight).

As far as the drugs, I will let someone else tackle them.

I have been VERY basic about this topic, however taking an EMT-B course this is probably all you really need to know till your done school and have time to read up on it more in depth.

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Posted · Report post

Alpha receptors are primarily affected by the presence/absence of Norepinephrine. Alpha-1 causes vasoconstriction predominantly. Alpha-2 causes the release of norepinephrine to be halted. The negative feedback mechanism that is responsible for this keeps your blood pressure from going to high when you are placed under stress.

Beta receptors are located preferrentially. Beta-1 in the cardiac tissue, and beta-2 in the smooth muscle. Beta-2 is commonly referred to as a smooth muscle relaxant, but that is only part of the effect. There is also a beta-3 receptor that is responsible for gluconeogenesis, and glycogenolysis when stimulated. This is a poorly understood mechanism presently, but the effects of any of the sympathomimetic drugs make it apparent what the beta-3 receptor is doing.

As for drugs:

Alpha-1: Norepinephrine (Levophed), and Dopamine at higher doses, epinephrine

Alpha-2: Norepinephrine

Beta-1: Dopamine at typical doses (5-10 mcg/kg/min), epinephrine, dobutamine

Beta-2: Epinephrine, Albuterol, Terbutaline

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Posted · Report post

Okay, I don't really have anything better to do right now, so I'll take a shot at this...

First of all, the concept of a receptor. A receptor is basically a protein in a cell (usually in a cell membrane, but doesn't have to be (eg. NO and steroid receptors). When a ligand (an agonist) meets the receptor, the protein changes its physical conformation, making it more or less likely to do something else, eg. catalyze something, open an ion channel.

Antagonists bind to receptors like agonists, but without doing anything, effectively blocking them.

In the discussion of the receptors of the autonomic nervous system, we have a few types, classified by 1) their innervation (sympathetic vs. parasympathetic) and 2) their neurotransmitter. A neurotransmitter is the chemical material a nerve secretes and serves as a ligand for the receptor on the innervated organ. In short, the sympathetic nervous system is the gas pedal, the parasympathetic nervous system is the break (not universal*).

For (extreme) simplification, we can say that the neurotransmitter for the parasympathetic nervous system is acetylcholine, but epinephrine/norepinephrine for the sympathetic nervous system.

So, to the actual question, the receptors. I won't waste time on the biochemical properties, as they are irrelevant to the question (if you want, I can make another post on those):

Sympathetic. Alpha and beta. Norepinephrine and epinephrine work on both, but norepinephrine works much better on alfa and epinephrine on beta. Most actual sympathetic nerve fibers secrete norepinephrine, but the adrenal glands, which are classified as a part of the sympathetic nervous system, secrete mainly epinephrine. I'm skipping sympathetic cholinergic receptors on purpose.

Alfa1: Stimulatory. Think smooth muscle contraction to contract arteries almost everywhere (except in skeletal muscle).

Alfa2: Found on nerves in the GI tract, inhibit the release of their neurotransmitter, acetylcholine. I.e. inhibit the parasympathetic nervous system in the GI tract, as mobey said.

Beta1: Stimulatory. Found in the heart. See above post from mobey.

Beta2: Relaxant, most importantly in the lungs (bronchodilation), coronary arteries (vasodilation) and arteries skeletal muscle (also vasodilation).

Beta3: Stimulates the release of stored energy in fat cells.

Parasympathetic. All cholinergic, meaning, their ligand is acetylcholine. Divided into two, nicotinic and muscarinic. What's important here is that the muscarinic ones are sensitive to atropine as an antagonist (one will usually not try to block nicotinic receptors). Heart and smooth muscle have muscarinic receptors. Skeletal muscle nicotinic. We usually don't administer acetylcholine (for similar reasons as we don't like to block nicotinic receptors), but we can make the acetylcholine stay a little longer with estigmin (physostigmine - spelling?).

An example of how this whole thing works together is the fight or flight response. Epinephrine (adrenaline) is secreted as a response to danger. The heart races (beta1), the coronary arteries dilate to supply the heart muscle (beta2), the bronchii dilate (beta2), the fat cells release energy (beta3), the arteries in skeletal muscle dilate to get energy there (beta2), arteries elsewhere constrict to focus blood flow (and energy) to skeletal muscle and the heart.

So, we can stimulate or block those receptors by administrating the same chemicals the body uses as neurotransmitters. An example would be when we want to get the heart going, we administer epinephrine (stimulate the beta1 receptors on the heart, step on the gas pedal) and atropine (block the effect of the parasympathetic nervous system on the muscarinic, cholinergic receptors, take the foot of the break).

So, yeah. Hope this post is not too confusing. I was trying to give a good picture without going into too much detail...

*The GI tract for example, is stimulated by the parasympathetic nervous system and its activity decreased by the sympathetic one - makes sense in a fight or flight response to divert energy from things like that and to more important things).

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Posted · Report post

I have nothing constructive to add but this, this is exactly what this forum is about. Great Question Anthony I needed a refresher on these anyway.

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Posted · Report post

That was a great question. I have been trying to figure it out to. This helped me out. Angela

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Posted · Report post

Thanks guys. This is an excellent thread. Reading it has helped me better understand the medications that I'm leaning in my EMT-I class. :D Thanks for the question, Anthony.

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Posted · Report post

So now understanding how the system works you can start to relate some of your medication types, think about how the following classes of meds would affect Pt. presentation:

Beta Blockers (Metoprolol is a common one)

Sympathomemetics (Epinephrine, Ventolin.)

Alpha Blockers (k I don't know any off hand)

If the parasympathetic system uses cholinergic neurotransmittors what affect would an anticholinergic drug such as Atrovent do?

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