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Eberhard Ritz - One of the best experts on this subject based on the ideXlab platform.
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oxidative stress after Uninephrectomy alters heart morphology in the apolipoprotein e mouse
Journal of Hypertension, 2008Co-Authors: Grzegorz Piecha, Nadezda Koleganova, Marie-luise Gross, Aman Geldyyev, Eberhard RitzAbstract:Objective Even minor reduction in glomerular filtration rate accelerates atherogenesis and increases cardiovascular risk. The current study on the apolipoprotein E -/- mouse was designed to investigate whether nephron reduction by Uninephrectomy causes cardiac remodeling and whether this is prevented by antioxidative treatment. Methods We randomized apolipoprotein E -/- mice to undergo Uninephrectomy or sham operation and subsequent treatment with either Tempol, Ebselen, Trandolapril, or a combination of Tempol and Trandolapril. After 12 weeks, the experiment was terminated by perfusion fixation under anesthesia. The myocardium was analyzed by morphometry. Additionally, the expression of endothelial nitric oxide synthase, transforming growth factor-beta1, vascular endothelial growth factor, flt-1, collagen I and presence of nitrotyrosine were assessed using immunohistochemistry or western blotting. Results Untreated uninephrectomized animals had lower capillary length density and higher volume fraction of interstitial tissue in the myocardium and bigger plaques in aorta compared with those who underwent sham operation. These changes did not develop in uninephrectomized animals treated with Tempol, Ebselen, Trandolapril, or Tempol + Trandolapril. In untreated uninephrectomized mice, the presence of nitrotyrosine and the expression of transforming growth factor-beta1, vascular endothelial growth factor, and collagen I were more marked. This was ameliorated by Tempol, Ebselen, Trandolapril, and Tempol + Trandolapril. Conclusion We conclude that in the apolipoprotein E -/- mouse, even minor reduction in renal function, for example, by Uninephrectomy, causes remodeling of the heart. This was ameliorated to a similar extent by antioxidants and angiotensin-converting enzyme inhibition.
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Oxidative stress after Uninephrectomy alters heart morphology in the apolipoprotein E -/- mouse.
Journal of hypertension, 2008Co-Authors: Grzegorz Piecha, Nadezda Koleganova, Marie-luise Gross, Aman Geldyyev, Eberhard RitzAbstract:Objective Even minor reduction in glomerular filtration rate accelerates atherogenesis and increases cardiovascular risk. The current study on the apolipoprotein E -/- mouse was designed to investigate whether nephron reduction by Uninephrectomy causes cardiac remodeling and whether this is prevented by antioxidative treatment. Methods We randomized apolipoprotein E -/- mice to undergo Uninephrectomy or sham operation and subsequent treatment with either Tempol, Ebselen, Trandolapril, or a combination of Tempol and Trandolapril. After 12 weeks, the experiment was terminated by perfusion fixation under anesthesia. The myocardium was analyzed by morphometry. Additionally, the expression of endothelial nitric oxide synthase, transforming growth factor-beta1, vascular endothelial growth factor, flt-1, collagen I and presence of nitrotyrosine were assessed using immunohistochemistry or western blotting. Results Untreated uninephrectomized animals had lower capillary length density and higher volume fraction of interstitial tissue in the myocardium and bigger plaques in aorta compared with those who underwent sham operation. These changes did not develop in uninephrectomized animals treated with Tempol, Ebselen, Trandolapril, or Tempol + Trandolapril. In untreated uninephrectomized mice, the presence of nitrotyrosine and the expression of transforming growth factor-beta1, vascular endothelial growth factor, and collagen I were more marked. This was ameliorated by Tempol, Ebselen, Trandolapril, and Tempol + Trandolapril. Conclusion We conclude that in the apolipoprotein E -/- mouse, even minor reduction in renal function, for example, by Uninephrectomy, causes remodeling of the heart. This was ameliorated to a similar extent by antioxidants and angiotensin-converting enzyme inhibition.
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Effects of testosterone on glomerular growth after Uninephrectomy.
Nephrology dialysis transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 1998Co-Authors: Martin Zeier, R. Schönherr, Kerstin Amann, Eberhard RitzAbstract:Background. Renal functional prognosis is consistently more adverse in male individuals with renal disease. Male animals develop more marked proteinuria and glomerulosclerosis in several models of renal damage. Renal and glomerular growth are important permissive factors for progression of renal failure. Purpose of the study. To investigate the influence of testosterone on renal and glomerular growth. Design. Renal compensatory growth after Uninephrectomy (UNX) was chosen as a model of renal growth. The effect of testosterone was assessed in control male, in orchidectomized (OX) male, and in ovariectomized (OV ) female SD rats. Observation time was 10 months. Measurements. Albuminuria by nephelometry; glomerular diameter, glomerular tuft area, renal zonal analysis by quantitative stereology. Testosterone and dihydroxytestosterone by gas chromatography and RIA. Results. In sham-operated male rats, testosterone administration did not change the (left) kidney:bodyweight ratio after Uninephrectomy. In contrast, in OX male rats, testosterone administration caused a significant increase in kidney:body-weight ratio and in albuminuria. In these animals, glomerular diameter and outer stripe width were significantly lower in OX rats than in sham-operated controls. Glomerular volume and outer stripe width in OX animals were significantly higher after Uninephrectomy (UNX) and were further increased in OX-UNX animals by administration of testosterone. Similar effects on glomerular diameter, cortical width (single) kidney:body-weight ratio were seen when OV female rats were treated with testosterone. Conclusion. After gonadal ablation, administration of testosterone amplifies compensatory glomerular and tubular growth in uninephrectomized male and female rats, i.e. testosterone is a permissive factor. Stimulation of glomerular growth may favour development of glomerulosclerosis.
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The effect of Uninephrectomy on progression of renal failure in autosomal dominant polycystic kidney disease.
Journal of the American Society of Nephrology : JASN, 1992Co-Authors: Martin Zeier, S Geberth, A Gonzalo, Dominique Chauveau, Jean-pierre Grünfeld, Eberhard RitzAbstract:The evolution of renal failure was compared in 47 patients (21 male, 26 female) with autosomal dominant polycystic kidney disease (ADPKD) in Germany, France, Spain, and Portugal who had undergone Uninephrectomy (UNX) (median age at Uninephrectomy, 41 yr; range, 22 to 54) and 47 non-UNX matched controls. UNX was usually performed because of uncontrolled urinary tract infection (N = 30), stones (N = 8), trauma (N = 2), or hemorrhage (N = 7). Median serum creatinine at UNX was 2.1 mg/dL (0.9 to 4.3). Twenty-eight of the 47 uninephrectomized patients progressed to end-stage renal failure. When the age at renal death was evaluated by survival analysis, only minor and nonsignificant acceleration was seen in the uninephrectomized patients (median, 50 yr; p25 = 43.6 yr; p75 = 58.3 yr, where p is the percentile) compared with non-UNX patients matched for age, sex, and serum creatinine at the time of UNX in the propositus (51.2 yr; p25 = 48.6 yr; p75 = 56.1 yr). In addition, the median interval for serum creatinine to rise from 4 to 8 mg/dL was similar in UNX (21.3 months) versus nonuninephrectomized ADPKD patients (21.9 months). Renal survival differed in the two genders. In females, no significant difference of age at renal death was found between UNX (median age, 51.6 yr) and non-UNX ADPKD patients (53.7 yr). In male UNX patients, age at renal death was slightly (but not significantly) less than in non-UNX patients (median age, 47.3 versus 52.7 yr). All male patients reaching end-stage renal failure before age 44 were severely hypertensive.
A Hishida - One of the best experts on this subject based on the ideXlab platform.
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Uninephrectomy prevents the ischemia-induced increase in renin activity.
Nephron, 1997Co-Authors: A Kato, A Hishida, Issei Tanaka, Katsutoshi KomatsuAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic injury. The present work was performed to elucidate whether the beneficial effect of Uninephrectomy was associated with the modification of ischemia-induced changes in plasma or renal renin activity. A 60-min left renal artery occlusion was conducted in right nephrectomized (Nx) and sham-nephrectomized (Sham-Nx) rats. The decline in inulin clearance 48 h after ischemia was significantly less in Nx rats than in Sham-Nx animals (0.50 ± 0.10 vs. 0.052 ± 0.029 ml/min/kidney, p
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Uninephrectomy reduces apoptotic cell death and enhances renal tubular cell regeneration in ischemic ARF in rats.
American Journal of Physiology-Renal Physiology, 1996Co-Authors: T Nakajima, T Miyaji, A Kato, N Ikegaya, T Yamamoto, A HishidaAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic renal injury functionally and morphologically. In this study we investigated the effects of Uninephrectomy on apoptotic renal cell death and tubular regeneration in ischemic acute renal failure (ARF) in rats. Unilateral ischemic injury was provoked by a 60-min left renal artery occlusion in right-nephrectomized (Nx) and sham-nephrectomized (sham-Nx) rats. Uninephrectomy attenuated tubular damage 48 h following the renal ischemia Apoptotic cells were found in renal tissue as early as 3 h after reperfusion and increased in number by 12 h. The “ladder” pattern of DNA fragments on agarose gel electrophoresis was also apparent in ischemic kidney. Uninephrectomy reduced apoptotic cells and DNA fragmentation. The expression of proliferating cell nuclear antigen (PCNA) could be seen 24 h after reperfusion and progressively increased thereafter PCNA expression in ischemic kidney was greater in Nx than sham-Nx rats at 24 h after renal reperfusion. These da...
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Uninephrectomy reduces apoptotic cell death and enhances renal tubular cell regeneration in ischemic ARF in rats.
The American journal of physiology, 1996Co-Authors: T Nakajima, T Miyaji, A Kato, N Ikegaya, T Yamamoto, A HishidaAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic renal injury functionally and morphologically. In this study we investigated the effects of Uninephrectomy on apoptotic renal cell death and tubular regeneration in ischemic acute renal failure (ARF) in rats. Unilateral ischemic injury was provoked by a 60-min left renal artery occlusion in right-nephrectomized (Nx) and sham-nephrectomized (sham-Nx) rats. Uninephrectomy attenuated tubular damage 48 h following the renal ischemia Apoptotic cells were found in renal tissue as early as 3 h after reperfusion and increased in number by 12 h. The "ladder" pattern of DNA fragments on agarose gel electrophoresis was also apparent in ischemic kidney. Uninephrectomy reduced apoptotic cells and DNA fragmentation. The expression of proliferating cell nuclear antigen (PCNA) could be seen 24 h after reperfusion and progressively increased thereafter PCNA expression in ischemic kidney was greater in Nx than sham-Nx rats at 24 h after renal reperfusion. These data suggest that Uninephrectomy reduces apoptotic cells and DNA fragmentation and enhances PCNA expression. The reduced apoptotic cell death and enhanced cell regeneration may be importantly involved in the Uninephrectomy-induced attenuation of ischemic acute renal failure in rats.
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Role of thromboxane A2 and prostacyclin in Uninephrectomy-induced attenuation of ischemic renal injury
Kidney international, 1995Co-Authors: A Kato, A Hishida, T NakajimaAbstract:Role of thromboxane A 2 and prostacyclin in Uninephrectomy-induced attenuation of ischemic renal injury. Contralateral Uninephrectomy attenuates unilateral renal ischemic injury. The present work was performed to elucidate whether the beneficial effect of Uninephrectomy was mediated through the modification of the actions of thromboxane A 2 (TxA 2 ) or prostacyclin. Unilateral ischemic injury was provoked by a 60-minute left renal artery occlusion in right nephrectomized (Nx) and in sham-nephrectomized (Sham-Nx) rats. Inulin clearance (C In ) of left kidney 48 hours after ischemia was significantly higher in the Nx group than in the Sham-Nx group (0.11 ± 0.07 vs. 0.00 ± 0.00 ml/min/kidney, P 2 content was greater in Sham-Nx rats than in Nx rats (29.5 ± 4.4 vs. 18.3 ± 1.7 pg/mg protein, P 1α between two ischemia groups. A thromboxane synthetase inhibitor, OKY-046 (100 mg/kg/day, i.p.), significantly increased C In 48 hours after ischemia (0.00 ± 0.00 vs. 0.17 ± 0.09 ml/min/kidney, P In and ischemic tubular damage between the Nx and Sham-Nx groups. OKY-046 also increased PCNA expression in the cortex and outer stripe in Sham-Nx animals. These data suggest that less production of intrarenal TxB 2 plays an important role for the Uninephrectomy-induced attenuation of ischemic renal damage and for the facilitation of tubular recovery.
T Nakajima - One of the best experts on this subject based on the ideXlab platform.
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Uninephrectomy reduces apoptotic cell death and enhances renal tubular cell regeneration in ischemic ARF in rats.
American Journal of Physiology-Renal Physiology, 1996Co-Authors: T Nakajima, T Miyaji, A Kato, N Ikegaya, T Yamamoto, A HishidaAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic renal injury functionally and morphologically. In this study we investigated the effects of Uninephrectomy on apoptotic renal cell death and tubular regeneration in ischemic acute renal failure (ARF) in rats. Unilateral ischemic injury was provoked by a 60-min left renal artery occlusion in right-nephrectomized (Nx) and sham-nephrectomized (sham-Nx) rats. Uninephrectomy attenuated tubular damage 48 h following the renal ischemia Apoptotic cells were found in renal tissue as early as 3 h after reperfusion and increased in number by 12 h. The “ladder” pattern of DNA fragments on agarose gel electrophoresis was also apparent in ischemic kidney. Uninephrectomy reduced apoptotic cells and DNA fragmentation. The expression of proliferating cell nuclear antigen (PCNA) could be seen 24 h after reperfusion and progressively increased thereafter PCNA expression in ischemic kidney was greater in Nx than sham-Nx rats at 24 h after renal reperfusion. These da...
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Uninephrectomy reduces apoptotic cell death and enhances renal tubular cell regeneration in ischemic ARF in rats.
The American journal of physiology, 1996Co-Authors: T Nakajima, T Miyaji, A Kato, N Ikegaya, T Yamamoto, A HishidaAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic renal injury functionally and morphologically. In this study we investigated the effects of Uninephrectomy on apoptotic renal cell death and tubular regeneration in ischemic acute renal failure (ARF) in rats. Unilateral ischemic injury was provoked by a 60-min left renal artery occlusion in right-nephrectomized (Nx) and sham-nephrectomized (sham-Nx) rats. Uninephrectomy attenuated tubular damage 48 h following the renal ischemia Apoptotic cells were found in renal tissue as early as 3 h after reperfusion and increased in number by 12 h. The "ladder" pattern of DNA fragments on agarose gel electrophoresis was also apparent in ischemic kidney. Uninephrectomy reduced apoptotic cells and DNA fragmentation. The expression of proliferating cell nuclear antigen (PCNA) could be seen 24 h after reperfusion and progressively increased thereafter PCNA expression in ischemic kidney was greater in Nx than sham-Nx rats at 24 h after renal reperfusion. These data suggest that Uninephrectomy reduces apoptotic cells and DNA fragmentation and enhances PCNA expression. The reduced apoptotic cell death and enhanced cell regeneration may be importantly involved in the Uninephrectomy-induced attenuation of ischemic acute renal failure in rats.
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Role of thromboxane A2 and prostacyclin in Uninephrectomy-induced attenuation of ischemic renal injury
Kidney international, 1995Co-Authors: A Kato, A Hishida, T NakajimaAbstract:Role of thromboxane A 2 and prostacyclin in Uninephrectomy-induced attenuation of ischemic renal injury. Contralateral Uninephrectomy attenuates unilateral renal ischemic injury. The present work was performed to elucidate whether the beneficial effect of Uninephrectomy was mediated through the modification of the actions of thromboxane A 2 (TxA 2 ) or prostacyclin. Unilateral ischemic injury was provoked by a 60-minute left renal artery occlusion in right nephrectomized (Nx) and in sham-nephrectomized (Sham-Nx) rats. Inulin clearance (C In ) of left kidney 48 hours after ischemia was significantly higher in the Nx group than in the Sham-Nx group (0.11 ± 0.07 vs. 0.00 ± 0.00 ml/min/kidney, P 2 content was greater in Sham-Nx rats than in Nx rats (29.5 ± 4.4 vs. 18.3 ± 1.7 pg/mg protein, P 1α between two ischemia groups. A thromboxane synthetase inhibitor, OKY-046 (100 mg/kg/day, i.p.), significantly increased C In 48 hours after ischemia (0.00 ± 0.00 vs. 0.17 ± 0.09 ml/min/kidney, P In and ischemic tubular damage between the Nx and Sham-Nx groups. OKY-046 also increased PCNA expression in the cortex and outer stripe in Sham-Nx animals. These data suggest that less production of intrarenal TxB 2 plays an important role for the Uninephrectomy-induced attenuation of ischemic renal damage and for the facilitation of tubular recovery.
A Kato - One of the best experts on this subject based on the ideXlab platform.
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Uninephrectomy prevents the ischemia-induced increase in renin activity.
Nephron, 1997Co-Authors: A Kato, A Hishida, Issei Tanaka, Katsutoshi KomatsuAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic injury. The present work was performed to elucidate whether the beneficial effect of Uninephrectomy was associated with the modification of ischemia-induced changes in plasma or renal renin activity. A 60-min left renal artery occlusion was conducted in right nephrectomized (Nx) and sham-nephrectomized (Sham-Nx) rats. The decline in inulin clearance 48 h after ischemia was significantly less in Nx rats than in Sham-Nx animals (0.50 ± 0.10 vs. 0.052 ± 0.029 ml/min/kidney, p
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Uninephrectomy reduces apoptotic cell death and enhances renal tubular cell regeneration in ischemic ARF in rats.
American Journal of Physiology-Renal Physiology, 1996Co-Authors: T Nakajima, T Miyaji, A Kato, N Ikegaya, T Yamamoto, A HishidaAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic renal injury functionally and morphologically. In this study we investigated the effects of Uninephrectomy on apoptotic renal cell death and tubular regeneration in ischemic acute renal failure (ARF) in rats. Unilateral ischemic injury was provoked by a 60-min left renal artery occlusion in right-nephrectomized (Nx) and sham-nephrectomized (sham-Nx) rats. Uninephrectomy attenuated tubular damage 48 h following the renal ischemia Apoptotic cells were found in renal tissue as early as 3 h after reperfusion and increased in number by 12 h. The “ladder” pattern of DNA fragments on agarose gel electrophoresis was also apparent in ischemic kidney. Uninephrectomy reduced apoptotic cells and DNA fragmentation. The expression of proliferating cell nuclear antigen (PCNA) could be seen 24 h after reperfusion and progressively increased thereafter PCNA expression in ischemic kidney was greater in Nx than sham-Nx rats at 24 h after renal reperfusion. These da...
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Uninephrectomy reduces apoptotic cell death and enhances renal tubular cell regeneration in ischemic ARF in rats.
The American journal of physiology, 1996Co-Authors: T Nakajima, T Miyaji, A Kato, N Ikegaya, T Yamamoto, A HishidaAbstract:Contralateral Uninephrectomy attenuates unilateral ischemic renal injury functionally and morphologically. In this study we investigated the effects of Uninephrectomy on apoptotic renal cell death and tubular regeneration in ischemic acute renal failure (ARF) in rats. Unilateral ischemic injury was provoked by a 60-min left renal artery occlusion in right-nephrectomized (Nx) and sham-nephrectomized (sham-Nx) rats. Uninephrectomy attenuated tubular damage 48 h following the renal ischemia Apoptotic cells were found in renal tissue as early as 3 h after reperfusion and increased in number by 12 h. The "ladder" pattern of DNA fragments on agarose gel electrophoresis was also apparent in ischemic kidney. Uninephrectomy reduced apoptotic cells and DNA fragmentation. The expression of proliferating cell nuclear antigen (PCNA) could be seen 24 h after reperfusion and progressively increased thereafter PCNA expression in ischemic kidney was greater in Nx than sham-Nx rats at 24 h after renal reperfusion. These data suggest that Uninephrectomy reduces apoptotic cells and DNA fragmentation and enhances PCNA expression. The reduced apoptotic cell death and enhanced cell regeneration may be importantly involved in the Uninephrectomy-induced attenuation of ischemic acute renal failure in rats.
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Role of thromboxane A2 and prostacyclin in Uninephrectomy-induced attenuation of ischemic renal injury
Kidney international, 1995Co-Authors: A Kato, A Hishida, T NakajimaAbstract:Role of thromboxane A 2 and prostacyclin in Uninephrectomy-induced attenuation of ischemic renal injury. Contralateral Uninephrectomy attenuates unilateral renal ischemic injury. The present work was performed to elucidate whether the beneficial effect of Uninephrectomy was mediated through the modification of the actions of thromboxane A 2 (TxA 2 ) or prostacyclin. Unilateral ischemic injury was provoked by a 60-minute left renal artery occlusion in right nephrectomized (Nx) and in sham-nephrectomized (Sham-Nx) rats. Inulin clearance (C In ) of left kidney 48 hours after ischemia was significantly higher in the Nx group than in the Sham-Nx group (0.11 ± 0.07 vs. 0.00 ± 0.00 ml/min/kidney, P 2 content was greater in Sham-Nx rats than in Nx rats (29.5 ± 4.4 vs. 18.3 ± 1.7 pg/mg protein, P 1α between two ischemia groups. A thromboxane synthetase inhibitor, OKY-046 (100 mg/kg/day, i.p.), significantly increased C In 48 hours after ischemia (0.00 ± 0.00 vs. 0.17 ± 0.09 ml/min/kidney, P In and ischemic tubular damage between the Nx and Sham-Nx groups. OKY-046 also increased PCNA expression in the cortex and outer stripe in Sham-Nx animals. These data suggest that less production of intrarenal TxB 2 plays an important role for the Uninephrectomy-induced attenuation of ischemic renal damage and for the facilitation of tubular recovery.
Grzegorz Piecha - One of the best experts on this subject based on the ideXlab platform.
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oxidative stress after Uninephrectomy alters heart morphology in the apolipoprotein e mouse
Journal of Hypertension, 2008Co-Authors: Grzegorz Piecha, Nadezda Koleganova, Marie-luise Gross, Aman Geldyyev, Eberhard RitzAbstract:Objective Even minor reduction in glomerular filtration rate accelerates atherogenesis and increases cardiovascular risk. The current study on the apolipoprotein E -/- mouse was designed to investigate whether nephron reduction by Uninephrectomy causes cardiac remodeling and whether this is prevented by antioxidative treatment. Methods We randomized apolipoprotein E -/- mice to undergo Uninephrectomy or sham operation and subsequent treatment with either Tempol, Ebselen, Trandolapril, or a combination of Tempol and Trandolapril. After 12 weeks, the experiment was terminated by perfusion fixation under anesthesia. The myocardium was analyzed by morphometry. Additionally, the expression of endothelial nitric oxide synthase, transforming growth factor-beta1, vascular endothelial growth factor, flt-1, collagen I and presence of nitrotyrosine were assessed using immunohistochemistry or western blotting. Results Untreated uninephrectomized animals had lower capillary length density and higher volume fraction of interstitial tissue in the myocardium and bigger plaques in aorta compared with those who underwent sham operation. These changes did not develop in uninephrectomized animals treated with Tempol, Ebselen, Trandolapril, or Tempol + Trandolapril. In untreated uninephrectomized mice, the presence of nitrotyrosine and the expression of transforming growth factor-beta1, vascular endothelial growth factor, and collagen I were more marked. This was ameliorated by Tempol, Ebselen, Trandolapril, and Tempol + Trandolapril. Conclusion We conclude that in the apolipoprotein E -/- mouse, even minor reduction in renal function, for example, by Uninephrectomy, causes remodeling of the heart. This was ameliorated to a similar extent by antioxidants and angiotensin-converting enzyme inhibition.
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Oxidative stress after Uninephrectomy alters heart morphology in the apolipoprotein E -/- mouse.
Journal of hypertension, 2008Co-Authors: Grzegorz Piecha, Nadezda Koleganova, Marie-luise Gross, Aman Geldyyev, Eberhard RitzAbstract:Objective Even minor reduction in glomerular filtration rate accelerates atherogenesis and increases cardiovascular risk. The current study on the apolipoprotein E -/- mouse was designed to investigate whether nephron reduction by Uninephrectomy causes cardiac remodeling and whether this is prevented by antioxidative treatment. Methods We randomized apolipoprotein E -/- mice to undergo Uninephrectomy or sham operation and subsequent treatment with either Tempol, Ebselen, Trandolapril, or a combination of Tempol and Trandolapril. After 12 weeks, the experiment was terminated by perfusion fixation under anesthesia. The myocardium was analyzed by morphometry. Additionally, the expression of endothelial nitric oxide synthase, transforming growth factor-beta1, vascular endothelial growth factor, flt-1, collagen I and presence of nitrotyrosine were assessed using immunohistochemistry or western blotting. Results Untreated uninephrectomized animals had lower capillary length density and higher volume fraction of interstitial tissue in the myocardium and bigger plaques in aorta compared with those who underwent sham operation. These changes did not develop in uninephrectomized animals treated with Tempol, Ebselen, Trandolapril, or Tempol + Trandolapril. In untreated uninephrectomized mice, the presence of nitrotyrosine and the expression of transforming growth factor-beta1, vascular endothelial growth factor, and collagen I were more marked. This was ameliorated by Tempol, Ebselen, Trandolapril, and Tempol + Trandolapril. Conclusion We conclude that in the apolipoprotein E -/- mouse, even minor reduction in renal function, for example, by Uninephrectomy, causes remodeling of the heart. This was ameliorated to a similar extent by antioxidants and angiotensin-converting enzyme inhibition.
