Animal models of hypertension: an overview.

Although the importance of the human kidney in a variety of disease states is well recognised, the exact mechanisms involved remain unclear. Animal disease models suggest that while high local concent

Cytokine-stimulated nitric oxide production in the human renal proximal tubule and its modulation by natriuretic peptides: A novel immunomodulatory mechanism?

Mycophenolate mofetil reduces renal cortical inducible nitric oxide synthase mRNA expression and diminishes glomerulosclerosis in MRL/lpr mice

Over-expression of iNOS is implicated in the pathogenesis of glomerulonephritis in animal models of systemic lupus erythematosus. The aim of this study was to evaluate the effect of aminoguanidine, a selective inhibitor of iNOS, for the protection from glomerulosclerosis in NZB/W F1 mice. Female NZB/W F1 mice (n = 8) were treated with aminoguanidine (1 g/l) in drinking water for 4 months starting at age 2 months before the onset of glomerulonephritis. Controls were age- and sex-matched mice (n = 10) without aminoguanidine treatment. By glomerular microdissection and reverse-transcription competitive polymerase chain reaction, we found that glomerular iNOS/beta-actin and TGF-beta1/beta-actin mRNA ratios were reduced 15.1% (P<0.05) and 61.3% (P<0.01), respectively, in aminoguanidine-treated mice. Aminoguanidine significantly reduced the glomerular iNOS staining, urinary nitrite production and degree of glomerulosclerosis. In addition, the glomerular volume and mean glomerular cell number were reduced 33.2% (P<0.01) and 32.8% (P<0.01), respectively. Likewise, the urinary proteinuria was also significantly reduced by aminoguanidine. These results indicate that administration of aminoguanidine may reduce the progression of glomerulosclerosis in NZB/W F1 mice, possibly through inhibition of glomerular nitric oxide production.

Aminoguanidine reduces glomerular inducible nitric oxide synthase (iNOS) and transforming growth factor-beta 1 (TGF-β1) mRNA expression and diminishes glomerulosclerosis in NZB/W F1 mice

Expression of the inducible form of nitric oxide synthase (iNOS) has been found to be up-regulated in cytokine-stimulated mesangial cells (MC) and in experimental glomerulonephritis Since direct toxicity of nitric oxide (NO) has been implicated in damage of bacteria, neoplastic and intact pancreatic cells, we investigated whether NO is cytotoxic to cultured MC, which may be relevant to pathogenesis of glomerular injury MC isolated from rat glomeruli generated substantial amounts of nitrite, the stable NO end-product, when cells were stimulated with IL-1beta and tumour necrosis factor-alpha (TNF-alpha) Total DNA synthesis was significantly reduced in the presence of IL-1beta and TNF-alpha, and this effect was completely reversed by N(G)-monomethyl-L-arginine (L-NMMA), an inhibitor of iNOS Stimulation of MC with IL-1beta and TNF-alpha caused remarkable toxicity to these cells, measured by the MTT test (3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide cleavage, specific cytotoxicity 415 +/- 203%), and much less prominent MC lysis (3H-thymidine release, specific cytolysis 115 +/- 53%) Toxic effects of cytokines were fully reversible by the iNOS inhibitor Lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma), but not IL-1beta and TNF-alpha, induced rat peritoneal macrophages to produce large amounts of nitrite In co-culture, such prestimulated macrophages had significantly cytotoxic (MTT test 629 +/- 199%) and cytolytic (3H-thymidine release 579 +/- 138%) effects on MC Again, this toxicity was totally inhibited in the presence of L-NMMA We conclude from these results that cytokine-stimulated generation of NO by MC or macrophages is directly toxic to MC, and may play a role in pathogenesis of glomerular injury involving mesangiolysis

Cytotoxic effect of autocrine and macrophage‐derived nitric oxide on cultured rat mesangial cells

A wealth of evidence shows that nitric oxide can modulate the autoregulation of renal blood flow, the glomerular surface area available for filtration, the glomerulotubular feedback response, and the release of renin. From an integrative point of view, inhibition of nitric oxide synthesis will alter the function of all of these homeostatic mechanisms and impair the pressure-induced natriuresis secondary to increases in intrarenal vascular resistance and tubular sodium reabsorption. These effects, along with an elevation of both total peripheral resistance and vascular tone of the capacitance vessels, are the most likely determinants of the volume-dependent elevation of blood pressure (ie, salt-sensitive hypertension) that occurs during partial inhibition of nitric oxide synthesis. This observation has important physiological and pathologic implications because it shows for the first time that the blockade of a single endogenous vasodilator substance can produce a sustained increase in blood pressure that can be influenced by changes in blood volume. Because of these characteristics, this review emphasizes in particular the characteristics of the nitric oxide synthesis pathway and briefly describes several known methods of increasing the biologic activity of nitric oxide; these methods eventually may be modified and used as therapeutic interventions in humans with deficient nitric oxide synthesis.

Nitric oxide and renal function.

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Nitric oxide and renal function.