Cirrhosis serum induces a nitric oxide-associated vascular hyporeactivity of aortic segments from healthy rats in vitro

Schmandra, T. C.; Folz, Ina C.; Kimpel, Michael; Fleming, Ingrid; Holzer, Katharina; Hanisch, E.

doi:10.1097/00042737-200108000-00014

Cited by 7 publications

(12 citation statements)

References 24 publications

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“…Taking into account that upon HSV intranasal infection, we observed that in the lungs these cells stain positively for NOS-II, we decided to investigate if they were susceptible to AG inhibition of NO production. AG has been widely used as selective inhibitor of NOS-II activity [Gardiner et al, 1996;Lecanu et al, 1998;Guc, 1999;Neufeld et al, 1999Neufeld et al, , 2002Schmandra et al, 2001]. First, we observed that AG treatment was able to block, in a dose-dependent way, LPS plus IFN-g-induced NO production in cultures of cells obtained from bronchoalveolar washings (Fig.…”

Section: Ag Inhibits No Production In Vitro and Ex Vivomentioning

confidence: 70%

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Early inhibition of nitric oxide production increases HSV‐1 intranasal infection

Gamba

Cavalieri

Courrèges

et al. 2004

Journal of Medical Virology

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Here, we studied the role of nitric oxide (NO) production during the first steps of the respiratory infection of BALB/c mice with herpes simplex virus type 1 (HSV-1), strain F. Nitric oxide synthase II (NOS-II) mRNA and protein were detected by reverse transcription (RT)-PCR and dot blot, respectively in samples of lungs and turbinates early post-infection (p.i.). Immunohistochemical analysis revealed pulmonar macrophages and PMN expressing NOS-II in the lungs of infected animals. Animals intranasally treated with aminoguanidine (AG), a NOS inhibitor, during the first steps of infection, showed a dose-dependent increase in pneumonitis compared to controls. Viral titres in turbinates, lungs, and brains were higher in AG treated mice. Finally, histopathology studies revealed a stronger inflammation in eyes, and lungs of these animals. Taken together, these results suggest a role of NO in controlling primary HSV intranasal infection.

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Section: Ag Inhibits No Production In Vitro and Ex Vivomentioning

confidence: 70%

“…AG has been largely used as a selective NOS-II inhibitor [Gardiner et al, 1996;Lecanu et al, 1998;Guc, 1999;Neufeld et al, 1999Neufeld et al, , 2002Schmandra et al, 2001]. Mice were separated in different experimental groups according to the amount of AG received.…”

Section: Aminoguanidine (Ag) Treatment Of Infected Micementioning

confidence: 99%

Early inhibition of nitric oxide production increases HSV‐1 intranasal infection

Gamba

Cavalieri

Courrèges

et al. 2004

Journal of Medical Virology

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“…Taking into account that upon antigen inoculation, we observed the expression of NOS-II in turbinates and lungs, we decided to investigate the effect of inhibiting NO production on the antigen-specific immune response. For this purpose, we decided to use AG, taking into account that this compound has been widely used as selective inhibitor of NOS-II activity [21][22][23][24][25][26][27][28]. We observed that AG treatment was able to block, in a dose-dependent way, LPS plus IFN-␥-induced NO production in cultures of cells obtained from pulmonar washings (Fig.…”

Section: Nos-2 Activation In Turbinates and Lungs Obtained From Inocumentioning

confidence: 99%

“…For this purpose, we used aminoguanidine (AG), a drug that has been largely used as a selective NOS-II inhibitor [21][22][23][24][25][26][27][28].…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide modulation of the immune response against cholera toxin-adjuvated ovalbumin administered by the intranasal route

et al. 2004

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“…NO has been widely implicated in the decreased vascular response to endogenous vasoconstrictors, a generalized phenomenon observed in clinical and experimental cirrhosis, in the setting of elevated circulating levels of vasoconstrictors [29,31,33,37,38], although the mechanisms by which this happens are not completely elucidated. The present study also shows a decrease in renal response to PHE at 15 and 21 days after BDL, coexisting with an increase in urinary nitrite excretion.…”

Section: Figure 6 Representative Nitrotyrosine Expression In the Innementioning

confidence: 99%

Effects of chronic L-NAME on nitrotyrosine expression and renal vascular reactivity in rats with chronic bile-duct ligation

et al. 2008

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In liver cirrhosis, elevated levels of NO and ROS (reactive oxygen species) might greatly favour the generation of peroxynitrite. Peroxynitrite is a highly reactive oxidant and it can potentially alter the vascular reactivity and the function of different organs. In the present study, we evaluated whether peroxynitrite levels are related to the progression of renal vascular and excretory dysfunction during experimental cirrhosis induced by chronic BDL (bile-duct ligation) in rats. Experiments were performed at 7, 15 and 21 days after BDL in rats and in rats 21 days post-BDL chronically treated with L-NAME (N(G)-nitro-L-arginine methyl ester). Sodium balance, BP (blood pressure), basal RPP (renal perfusion pressure) and the renal vascular response to PHE (phenylephrine) and ACh (acetylcholine) in isolated perfused kidneys were measured. NO levels were calculated as 24-h urinary excretion of nitrites, ROS as TBARS (thiobarbituric acid-reacting substances), and peroxynitrite formation as the renal expression of nitrotyrosine. BDL rats had progressive sodium retention, and decreased BP, RPP and renal vascular responses to PHE and ACh in the time following BDL. They also had increasing levels of NO and ROS, and renal nitrotyrosine accumulation,especially in the medulla. All of these changes were either prevented or significantly decreased by chronic L-NAME administration. In conclusion, these results suggest that the increasing levels of peroxynitrite might contribute to the altered renal vascular response and sodium retention in the development of the experimental biliary cirrhosis. Moreover, the beneficial effects of decreasing NO synthesis are, at least in part, mediated by anti-peroxinitrite-related effects.

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Cirrhosis serum induces a nitric oxide-associated vascular hyporeactivity of aortic segments from healthy rats in vitro

Cited by 7 publications

References 24 publications

Early inhibition of nitric oxide production increases HSV‐1 intranasal infection

Early inhibition of nitric oxide production increases HSV‐1 intranasal infection

Nitric oxide modulation of the immune response against cholera toxin-adjuvated ovalbumin administered by the intranasal route

Effects of chronic L-NAME on nitrotyrosine expression and renal vascular reactivity in rats with chronic bile-duct ligation

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