Differential effects of nitric oxide on the activity of prostaglandin endoperoxide H synthase-1 and -2 in vascular endothelial cells

摘要: A number of studies have demonstrated that prostacyclin and nitric oxide (NO) regulate blood pressure, flow platelet aggregation. In this paper, we examined the possible relationship between NO prostaglandin endoperoxide H synthase (PGHS)-1 -2 activities in cultured bovine aortic endothelial cells. non-activated condition cells expressed PGHS-1 activity alone. When these were pretreated with aspirin to inactivate their then activated by serum phorbol ester (TPA) for 6 h, PGHS-2 The PGHS was assessed generation 6-ketoprostaglandin F1alpha (6-ketoPGF1alpha), a stable metabolite prostacyclin, after treatment arachidonic acid. simultaneous addition NOC-7, donor, acid did not affect production 6-ketoPGF1alpha cells, but attenuated it PGHS-2-expressed inhibitory effect NOC-7 on dose dependent, different effects isozymes also observed other donors. To confirm carried out an ex vivo perfusion assay aorta isolated from normal lipopolysaccharide (LPS)-treated rats. aortae rats, where dominant expression expected, donor activity, while LPS-treated dominantly expressed, dramatically inhibited suggesting suppressed mediated cyclic GMP (cGMP), since (a) methylene blue, inhibitor soluble guanylate cyclase abolish (b) 8-Br-cGMP, permeable cGMP analogue, failed mimic These data suggest dependent rate