Resveratrol (trans-3,4′,5-trihydroxystilbene, Rsv) is a small polyphenol molecule present in a large variety of plant species such as mulberries, peanuts and grapes. Rsv was largely utilized by Asian medicine for treatment of fungal, inflammatory, hypertensive, allergic, cancer and lipid diseases. Nowadays it is used in “natural medicine” and widely consumed by public as dietary supplementation due to its antioxidant properties. Despite various molecular targets have been proposed, AMP-activated protein kinase (AMPK) and NAD+-dependent histone deacetylase sirtuin 1 (SIRT1) are considered as the main effectors for Rsv actions. Rsv-induced SIRT1 activation would mediate anti-inflammatory by downregulation of NF-kB and COX2 expression and activity. Rsv-induced AMPK would decrease lipogenic genes expression. We have previously shown that both, COX2 expression and activity and remodeling of cell membranes are key factors for adaptation and survival of renal cells subjected to abrupt changes of environmental osmolality. In the present work, we evaluated whether Rsv affects such survival pathways. To do this, lipid profile and synthesis, determined by incorporation of [U-14C]-glycerol to lipid molecules, and COX2 expression were evaluated in cultures of the renal epithelial cell line MDCK incubated in NaCl-hyperosmotic media (~550 mOsm) without or with 100 􀀀M Rsv for 0, 6, 12, 24 48 and 72 h. After treatment, cells were collected, counted and viability determined. Lipids were extracted by Bligh-Dyer and separated by TLC. COX2 expression was assessed by western blot. Both lipid synthesis and COX2 expression were induced after 24, 48 and 72 h of hyperosmolar treatment, and both processes were harmed by Rsv from early time of treatment. Cell number recovered after Rsv was significant lower. These preliminary results suggest that in renal cells Rsv abolished protective mechanism against osmotic stress. Key words: resveratrol; osmoprotection; renal cells.