Messing with alpha-2 is probably the most tricky area, I get around the confusion by holding on tightly to certain trends.
Smooth muscles: Alpha 2 receptors are directly on them ("post synaptic"). In the CNS and the Heart (which isnt smooth muscle) Alpha 2 receptors are pre-synaptic and serve as a safety mechanism which I will mention later.
I always go with this for smooth muscle:
Alpha receptors (1 & 2) CONSTRICT.
Beta receptors (1 & 2) RELAX (dilate)
That means smooth muscle constricts by both Gq and Gi mechanisms, which can be confusion when thinking of Gi, basically the alpha subunit opposes the Gs inhibition of myosin light chain kinase, and the beta/gamma subunit actually stimulate Phospholipase C (support Gq function)
Smooth muscle DILATES by Gs mechanism.
So;
#1. NO. Blocking both alphas--> dilation. Th problem with MOA + tyramine = Hypertension, this is what you are managing.
#2. This can go either way, there is a risk of severe reflex tachycardia if correcting the hypertension too quickly, which is exacerbated by the alpha 2 blockage (which at the heart would facilitate increased release of NE), and Selective Alpha 1 blocker wouldn't carry as much risk of severe tachycardia. I still think the DOC for hypertensive crisis is generally alpha blockers.
#3. Pheochromocytoma: Alpha blockers, and Beta Blockers. Alpha blockers is correct, beta blockers is correct, using both is also correct usage.
#4. ? Not sure.
Now, the point of Alpha 2 receptors in the CNS I believe is to somewhat prevent excess vasoconstriction to vital organs, in conditions in which there is a huge surge of Epi. Large doses will activate alpha 2 in the cns and try to oppose all the sympathetic activity and constriction that would completely cut off blood supply to those organs and cause ischemic injury... (roughly some concept like that was outline in a kaplan video I saw, cant remember the details), the Beta 2 effect should only dilate arteries going to skeletal muscle, so no help there to keep other organs perfused.
The direct effect of alpha 2 receptors on smooth muscle is still constriction though.
Alpha agonists --> Smooth muscle constriction --> Side effect impotence.
Alpha antagonists --> Smooth muscle dilation, hence treatment in impotence.
Even though paradoxically you might think, Alpha 2 agonist --> decreased sympathetic tone --> therefore erection is possible, so no impotence. Idk... this just isnt true.
The central/peripheral mechanisms I think are pretty clear, but it gets confused with drugs which are candidly grouped as "Alpha 2 agonist" (like clonidine) because it is not specified where it acts.
Clonidine (alpha 2 agonist) so you expect vasoconstriction (per my rules above), so why then is it used to treat hypertension, because it only acts centrally, in the CNS!
Yohimbine Alpha 2 blocker --> Expect Vasodilation, and thats what you get. Can you guess when its used for vasoconstriction? With autonomic failure, I suppose in that case its more central acting.
