ABSTRACT
Aim To investigate the effect of high-salt model of mouse thoracic aortic endothelial cells on the production of nitric oxide (NO) . Methods After preincubation of thoracic aortic endothelial cells with transient receptor potential vanilloid 4 (TRPV4) inhibitor HC067047, the effects of TRPV4 on NO production were studied by Ca2+and NO staining with calcium ion fluorescent probe Fluo-4 and NO fluorescent probe DAF-FM DA. The thoracic aortic endothelial cells were stimulated with a high salt concentration of 60 mmo! L"1 to detect Ca2+influx and NO production Compared with control group, suppression of TRPV4 inhibited Ca2+influx and NO production in thoracic aortic endothelial cells, and high salt conditions inhibited TRPV4-medicated Ca2+influx and NO production compared with mannitol under the same osmotic pressure. Conclusion In high salt state, the inhibition of TRPV4 channel leads to the decrease of Ca2+influx and the down-regulation of NO synthesis.