system
Given the following post, respond as if you're commenting on Reddit:
human
Beta-blockers help dilate the blood vessels, but yet EP and NE cause vasodilation when they attach to beta-2-adrenergic receptors. Does that mean there are little to no Beta-2 receptors in the peripheral vessels, or does it mean less catecholamines bind to alpha 1 and alpha 2 receptors?

I am posting here because I do want an explanation, but I'd like it said in terms any average student would understand, which I don't think ELI5 would be able to provide this time around. 

Edit: Thanks to all who have answered my question so far. I'm a nursing student taking Med-Surg (in my second semester out of four to take my NCLEX), which means for now a lot of the material is introductory, but so far I am understanding the material ~~well~~ decently.
gpt
I don't have time to provide a detailed answer at the moment, but the effect of Beta-andrenergic receptor antagonists is not to dilate blood vessels. In incredibly simplistic terms, alpha receptors are excitatory except in the GI, and beta receptors are inhibitory except in the heart. 


So, consider this: epinephrine binds to a B-receptor in a peripheral vessel. Since it's *inhibitory* to the smooth muscle in the vessel wall, that vessel will dilate. If epinephrine binds to a B-receptor in the heart, it will have an *excitatory* effect. Meaning it will have a positive chronotropic (increased heart rate) and positive inotropic (increased cardiac contractility) effect on the heart. 


Nonselective B blockers, such as propanolol, block these receptors. Which means that the effect on the heart will be decreased heart rate and decreased contractility, and a mild vasoconstrictive effect on blood vessels. 


But thats in pretty simplistic terms. Hope this helped!