You are absolutely right! I worded my response wrongly.
how about a little detail:
• a a2 receptors serve as autoreceptors to feedback inhibit adrenergic neurotransmission
– NE a stimulates a2 receptors that are localized on presynaptic nerve terminals
– a a2 receptors interact with G i proteins that will reduce NE release from nerve terminal
What this means is that while NE does stimulate a2 receptors, the stimulation acts to LOWER current levels of NE (norepinephrine). alot of our chemical/hormone systems rely on checks and balances to maintain consistent levels.
• (yohimbine)can block NE from interacting w/ a a2 receptors and then facilitate continued
release of NE by nerve terminals
– thus synaptic levels of NE rise, allowing further sympathetic stimulation of target site
(vasoconstriction, tachycardia, mydriasis)
What this means is that by blocking a2 receptors yohimbine effectively causes the continued release of norepinephrine.
I apologize for for wording the post the way I did but I was attempting to clarify what yohimbine does without confusing everyone with too much technical info.