I am actually alittle confused as well. FA says Beta- agonists stimulate insulin release while alpha-agonists inhibit insulin release...now they don't really specify alpha1/2 or beta 1/2...do all types effect insulin release or just specific ones?
For example, it wouldn't make sense for alpha 1 to inhibit insulin, since activating alpha1 --> Gq --> increase Ca2+
Alpha2 --> Gi --> decrease cAMP
Beta1&2 --> Gs--> increase cAMP (FA doesn't mention the effect of cAMP on insulin release, so we just assume that increase cAMP --> increase insulin secretion??? assuming this will be consistent with alpha2 effects)
Clarification would be nice...it would be nice to know the "why" behind it, rather than just memorize lol
Ok, you need to remember that the sensitivity of the adrenergic receptors are not equal. That is to say, beta receptors are more sensitive than alpha receptors (if you want the full spectrum it goes, from increasing to decreasing sensitivity, D receptors > B receptors > alpha receptors). Further, you have to also recall that B2 receptors, the one that works on the pancreas, is not innervated. Consequently Epinephrine is the main natural agonist. In contrast, the alpha2 receptors on the pancreas are innervated.
So, when I am running from a murderous fiend my S-ANS leads to both NE activation but ALSO stimulates my adrenals to release Epinephrine into my blood stream. This will result predominately in activation of my Liver to raise blood glucose so that my skeletal muscles, heart, brain, etc can obtain glucose while I am trying to survive. However, what good is glucose floating around in my blood? Well, it is ok for the insulin-independent uptake of glucose, but remember, my skeletal muscles need glucose too! and they will burn through their glycogen stores very quickly. Consequently, the high levels of Epinephrine in the bloodstream will also leads to stimulation of B2 receptors on the pancreas to allow for a slight increase in insulin so that I can make use of all the glucose I produce from my liver.
As a general point, ALL stress hormones (Cortisol, Epinephrine, Glucagon) must raise insulin levels to some extent, otherwise skeletal muscle would be unable to utilize the fruits of the liver's labor.
As you point out, alpha1 stimulation is nonsense if it is going to oppose insulin release; therefore, your intuition is correct: it is alpha2 stimulation that tends to reduce the release of insulin. However, we said that B receptors are more sensitive than alpha receptors; therefore, under what circumstance would this be important? Alpha2-agonists are used in the management of mild HTN (think Clonidine or methyldopa for pregnancy). However, if we use these drugs in a Diabetic, then we would expect an exacerbation since we will not only decrease their BP (which we want to do) but we will also further reduce their insulin levels.
Final consideration:
Alpha1 receptors - Think classic autonomic effects on vessels, GU, Eye, sex organs etc
Alpha2 receptors - Prejunctional terminals are KEY, but also that wrinkle about the pancreas as well as platelets (so, with the example above, expect alpha2 agonists to not be used in patients with increase clot risk)
B1 receptors - Anything to do with Heart (Pacemaker, muscle) AND kidney
B2 receptors - Essentially the opposite of NE effects since in the fight/flight response if NE dominated the system there would be unrestricted vasoconstiction (via alpha1) which would ultimately lock up the blood supply resulting in decrease BF to heart, muscle, brain etc; therefore, Epinephrine opposes alpha1 in these situations so I can get away from murderous people/things
