Having recently answered a couple of threads pertaining to EDH and EDHFs, it is apparent that a generalized discussion of the topic on researchgate may be overdue. 

Generally defined as the residual relaxant response resistant to inhibitors of NOS and COX, EDH regulates vascular tone more prominently as vessel size decreases. Thus, it is important for the regulation of vascular resistance and tissue blood flow. 

The field is frought with confusion, particularly to the non-expert, due partly the the highly heterogeneous nature of EDH (e.g. transferable factors vs gap junctions vs combinations of mechanisms). Even among experts there is huge debate concerning the mechanisms that drive EDH and its relevance in vivo, as well as "drugability"

This "question" is in my mind intended to act as a useful platform for general debate on the topic, whether physiological, pharmacological, methodological etc in nature.