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S Lamas

Publications and source records attributed to S Lamas.

78 records · Page 5Linked to original sources
PubMedDate not supplied

Oxidative and nitrosative stress in kidney disease: a case for cyclosporine A.

The immunosuppresor cyclosporine A (CsA) has been associated to human endothelial dysfunction and accelerated atherosclerosis. Sympathetic overactivity, relative deficiency of nitric oxide, TGFb-1, endothelin-1, reactive oxygen (ROS) and nitrogen species (RNS) and vasoconstrictor eicosanoids are mediators of vascular dysfunction associated to cyclosporine A. In CsA-treated cells (BAEC) an increase in reactive oxygen and nitrogen intermediates may lead to the intracellular formation of peroxynitrite. This agent could be one important mediator by which CsA produces an antioxidant-sensitive nitration of tyrosine, a marker for endothelial damage by nitrosative stress. Superoxide anion is the limiting factor in the formation of peroxynitrite in CsA-treated endothelial cells. Treatment with CsA may lead to the nitration of specific proteins such as manganese superoxide dismutase (MnSOD). We propose that peroxynitrite and tyrosine nitration may represent mechanisms of damage in pathophysiological situations where superoxide anion generation is increased.

Cyclosporine↗
PubMedDate not supplied

Recombinant human erythropoietin does not regulate the expression of endothelin-1 and constitutive nitric oxide synthase in vascular endothelial cells.

Erythropoietin (rHuEPO)-induced hypertension represents a clinical problem in hemodialysis units. However, the underlying molecular mechanisms of this side effect are still unclear. In order to assess the potential participation of the endothelial-derived vasoactive factors, nitric oxide and endothelin-1, bovine aortic endothelial cells were incubated in the presence of rHuEPO. The latter (0.1-10 U/ml, 1-24 h) did not modify the synthesis of nitric oxide and endothelin-1 or the expression of nitric oxide synthase and pre-pro-endothelin-1 mRNAs. These results suggest that endothelial-derived vasoactive factors are not a key component in the hypertensive response observed in certain patients after the administration of rHuEPO.

Animals↗
PubMedDate not supplied

Gentamicin treatment increases mesangial cell nitric oxide production.

Gentamicin-induced decreases in glomerular filtration rate have been associated with a marked decline in the glomerular capillary ultrafiltration coefficient which could be mediated by mesangial cell contraction. We have assessed a possible role of endogenous nitric oxide (NO) as a modulator of the proliferative and contractile effects of gentamicin on mesangial cells. NO synthesis and release, measured as nitrite production, were increased in the presence of gentamicin; this increase was blocked by coincubation with L-NAME. Mesangial cells treated with gentamicin, but not cells under control conditions, expressed mac-iNOS mRNA and presented positive immunoreactivity for mac-iNOS. Gentamicin induced a reduction of the planar surface area of cultured rat mesangial cells; cell treatment with gentamicin plus L-arginine significantly decreased the contractile effect of gentamicin. Gentamicin increased both [3H]thymidine incorporation into DNA and viable cell number; when L-arginine was added together with gentamicin, this abolished the effect of gentamicin on mesangial cell proliferation. The present studies demonstrate that gentamicin induces the expression of mac-iNOS and produces contraction and proliferation in mesangial cells. These actions seem to be modulated by mesangial NO synthesis and release.

Animals↗