So, Yohimbine is a non-selective alpha-antagonist (deactivates). Basically alpha1 and alpha2 receptors have differing effects.
Agonizing (activating) alpha-1 receptors causes an increased breakdown of c-AMP. Antagonizing a1 (like yohimbone does) will decrease the breakdown of c-AMP. In a typical situation and enzyme called phosphodiesterase (PDE) breaks down c-AMP. Viagra inhibits PDE and thus prevents the breakdown of c-AMP. Increased c-AMP causes an increase in Nitric Oxide in the brain, which increases blood flow.
The issue is that Alpha-2 agonists decrease epinephrine levels and induce sedation. Antagonists like Yohimbine thus increase ephedrine levels and increase vasoconstriction (temporarily) and has seemingly contradictory effects to alpha-1 blockade.
Most people seem to have more A1 than A2 receptors, so a lower dose of Y will activate A1 and very few A2 receptors - thus increasing cAMP. As the dose increases, more A2 receptors get activated, creating a self-attenuating effect. Taking too much will activate enough A2 receptors to overcome the effects of the A1 blockade and basically cause contradictory effects.
Another thing is that just taking Y by itself seems to cause an increase in insulin release in some studies. How's that for a gotcha?