I went down a long rabbit hole during my cardio module and read like 4 or more different physiology books trying to figure out the cardiovascular system. That is right, arterioles, capillaries, and venules supply tissues.
I could be wrong, but what I understood was:
Arterioles control the distribution (path) of blood flow to tissues. This is done via altering their resistance. So think of a bunch of valves, and you simply loosen the valves of arterioles in tissues you want to supply more blood to, and constrict them for tissues you want to not perfuse too much. What you have to consider is there are global responses (nervous system) and local factors that control the resistance. Take for example in exercise: You get sympathetic outflow so there is a kind of pan-constriction (increased TPR) of arterioles. However, the tissues that are metabolically active such as skeletal muscle and cardiac muscle produce vasodilatory metabolites to increase their flow.
Capillaries are involved in filtration or absorption of metabolites. Venules are involved in venous return.
The main role of ARTERY (so like aorta) is to serve as a sort of a chamber for the MAP (mean arterial pressure). Think of MAP as the potential energy for the entire system. The MAP must be preserved at all costs, because it's the driving force for the blood flow. Remember that the highest resistance is in the arterioles, and so there is a pressure drop there. If there is too low of a MAP, then the pressure drop from the arterioles will impede the continuity of the flow.
Edit just to add some more things I remembered: That's why when you go into shock and your BP goes too low, you get increased HR and TPR via vaso constriction. It's to preserve MAP.
Remember, MAP= CO x TPR. and CO= HR x SV.
So think about it this way: MAP= HR x SV x TPR
Now let's say you go into shock, in other words, too little MAP. You get SNS outflow, resulting in increased HR (b1 receptors on heart), increased SV (a1 venous constriction), and increased TPR (a1 constriction on arterioles).
You may be thinking why would you want to increase TPR which would lead to decreased perfusion of tissues. However, keep in mind that highly metabolic tissues (high priority tissues) will produce local metabolic effects to increase their own perfusion. Also, keep in mind that B2 receptors will be stimulated during SNS outflow to promote vasodilation of arterioles. It seems that this would counteract the increase in TPR, so my assumption is that arterioles supplying "higher priority tissues" may have more B2 receptor density.
