Much confusion arises in the field of agonist–effector supersensitivity phenomena due to the often encountered lack of discrimination between agonist disposition mechanisms functioning, in the system under study, as access barriers and as terminating mechanisms. Access barriers limit agonist approach to the receptor region and terminating mechanisms serve to remove agonist from the site of action. The assumption of a quantitative identity in these two functions is not often warranted and the effects inhibition of these processes have on the magnitude of effector responses and on their duration can differ strikingly, both qualitatively and quantitatively.