You are on the right track to a BASIC understanding of the ANS. It's easiest to think in terms of receptor and effect (affinity). Endogenous catecholamines often act different than exogenous ones (they can target receptors more specifically). Epi effects differently than norepi although there is a lot that is identical in the receptors they effect. Dopamine works on an entirely different set. Etc. The only way to know it is to read and re-read. Also, your last sentence is incorrect. A sympathetic agonist does not inhibit the parasympathetic branch, it just changes the clinical picture by emphasizing one branch of the ANS over another. Example: IV epinephrine effects Beta 1, 2, and Alpha 1 and 2 receptors. low doses can actually cause hypotension due to beta2 mediated skeletal muscle vasodilitation, high doses causes tachycardia, hypertension and a whole lot of other responses. Parasympathetic innervation is not blocked but progressivly overwhelmed as a result of exogenous epinephrine administration. Norepi acts nearly the same except there is no beta 2 agonism.