We have recently demonstrated that rotigaptide does not enhance endothelium-dependent or independent forearm arterial vasodilatation in healthy volunteers. However there may be a role for potentiating gap junctions under some circumstances. In animal models of myocardial infarction those treated with rotigaptide had significantly reduced infarction sizes. Endothelial dysfunction is central to the pathophysiology of diabetes and is responsible for the vascular complications associated with this condition. In animal models of diabetes reduced expression of connexins has been demonstrated with blunted response to EDHF, suggesting a link between endothelial dysfunction and gap junctions.