Raloxifene acutely stimulates nitric oxide release from human endothelial cells via an activation of endothelial nitric oxide synthase.

摘要: Raloxifene is a selective estrogen receptor modulator (SERM) clinically effective for the prevention of postmenopausal osteoporosis. Estrogen’s effect on cardiovascular diseases mainly dependent direct actions vascular wall. Since raloxifene has an endothelium-dependent relaxing effect, we studied effects this molecule nitric oxide (NO) release from cultured human umbilical vein endothelial cells. Clinically concentrations compound triggered rapid and dose-dependent NO Raloxifene-induced production was receptor-mediated mechanism, since it abolished by pure antagonist ICI 182,780. Treatment monolayers with not associated changes in synthase (eNOS) messenger RNA or protein, showing that does increase through transcriptional eNOS. Indeed, raloxifene-induced due to...