Autonomic drug help

[cmonkey]

I *think* I'm starting to get this, but I still don't think I have it quite right. I couldn't tell you any of this off the top of my head, so I don't think I get it. If I got it, I could explain it, I think. But:

Sympathomimetics/adrenergic agents mimic the sympathatic nervous system. There are two kinds of receptors, A and B. Each of these has two sub groups. Each subgroup exerts an effect on the SNS, one stimulating, one suppressing. You can affect the SNS in multiple ways, depending on what receptor group you are going after. So while there are two A receptors, A1 stimulates (treating hypotension), and A2 suppresses (treating htn).

Right? And then within this sympathomimetic group, the alpha and beta subgroups are further labeled as catacholamines or noncatacholamines, which stimulate the SNS. The sympatholytic group has adrenergic blockers adrenergic antagonists, which inhibit/BLOCK the SNS.

The PNS is even easier because there are fewer items:

parasympathomimetics (cholinergic agents, muscarinic agents) stimulate/MIMIC the rest and digest response.

parasympatholytics (anticholinergics, muscarinic blockers) inhibit/BLOCK the rest and digest response.

When a drug stimulates the SNS, it will inhibit the PNS, and vice versa. Is it that simple (but still so complicated)?

[Richard_Head]

You are on the right track to a BASIC understanding of the ANS. It's easiest to think in terms of receptor and effect (affinity). Endogenous catecholamines often act different than exogenous ones (they can target receptors more specifically). Epi effects differently than norepi although there is a lot that is identical in the receptors they effect. Dopamine works on an entirely different set. Etc. The only way to know it is to read and re-read. Also, your last sentence is incorrect. A sympathetic agonist does not inhibit the parasympathetic branch, it just changes the clinical picture by emphasizing one branch of the ANS over another. Example: IV epinephrine effects Beta 1, 2, and Alpha 1 and 2 receptors. low doses can actually cause hypotension due to beta2 mediated skeletal muscle vasodilitation, high doses causes tachycardia, hypertension and a whole lot of other responses. Parasympathetic innervation is not blocked but progressivly overwhelmed as a result of exogenous epinephrine administration. Norepi acts nearly the same except there is no beta 2 agonism.

[cmonkey]

THANK YOU! I feel like I've made headway since I posted, but still. Ugh. I ended up finding a lot of ppts and podcast lectures and watched those. If I have enough time to sit and think about it, I can generally come up with the right answer. Our tests are open book, but HARD, so I really want to have this down before our next test.

eta: inhibiting is less accurate than desensitizing, yes? Because that's more the effect on the PNS and SNS, preventing the receptors from reacting to a drug?