Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3216529 | Journal of Investigative Dermatology | 2011 | 8 Pages |
In endothelial function, prostacyclin (PGI2) is as important as nitric oxide (NO); however, no test assesses specifically the vascular function of endogenous PGI2. We hypothesized that PGI2 has a dominant role in cathodal current-induced vasodilation (CIV) described in human skin. We thus aimed to study, in physiological conditions, the PGI2 involvement in cathodal CIV in rats in order to use pharmacological blockers that could not be used in humans. CIV was reduced by cyclooxygenase (COX)-1 and PGI2 synthase (PGIS) and PGI2 receptor (IP) blockers, but was unchanged by COX-2 and NO synthase (NOS) blockers. The level of 6-ketoPGF1α present in skin biopsies, measured as endogenous PGI2, was increased by cathodal current stimulation, except under COX-1 and PGIS inhibition. This study provides evidence that cathodal CIV mainly relies on the release of PGI2 endogenously produced through the COX-1/PGIS pathway, and then acts on IP receptors to relax the cutaneous microvessels in healthy rats. In contrast, neither COX-2 nor NOS is involved in CIV and the endogenous PGI2 release by current stimulation. This finding shows that cathodal current stimulation could be a valuable method to assess the vascular function of endogenous PGI2 in healthy skin.