There are several classes of drugs currently in use for the therapeutic management of the glaucomas. Although the ocular hypotensive effects of these agents have been well characterized and described, little is known of their site of action and cellular mechanism. This review attempts to describe those cellular mechanisms that may be linked to the actions of several classes of antiglaucoma drugs. Special emphasis was placed on drug actions and 1) the adenylate cyclase system; 2) receptor-coupled phosphoinositide turnover; 3) prostaglandins and 4) ion transport processes. Models are presented depicting proposed cellular sites of the interaction of the antiglaucoma drugs with these cellular processes.