Resistance to renal damage by chronic nitric oxide synthase inhibition in the Wistar-Furth rat

1 Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, Pennsylvania; 2 Department of Nutrition, West Virginia University, Morgantown, West Virginia; and 3 Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida Submitted 23 Ju...

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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2006-01, Vol.290 (1), p.R66-R72
Hauptverfasser: Erdely, Aaron, Freshour, Gary, Baylis, Chris
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container_title American journal of physiology. Regulatory, integrative and comparative physiology
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description 1 Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, Pennsylvania; 2 Department of Nutrition, West Virginia University, Morgantown, West Virginia; and 3 Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida Submitted 23 June 2005 ; accepted in final form 25 August 2005 Chronic nitric oxide synthase inhibition (NOSI) causes chronic kidney disease (CKD) in the Sprague Dawley (SD) rat. We previously showed that the Wistar-Furth (WF) rats are resistant to several models of CKD and maintain renal nitric oxide (NO) production compared with SD rats, whereas low-dose NOSI caused progression of CKD in WF rats. Here, we evaluate the impact of high-dose chronic NOSI in WF and SD rats, as well as intrarenal responses to an acute pressor dose of NOSI in the normal WF. Rats were given N G -nitro- L -arginine methyl ester ( L -NAME) (150 and 300 mg/l for 6–10 wk) in the drinking water after an initial bolus tail vein injection. Both strains showed significant reductions in total NO production with chronic L -NAME. SD given 150 mg/l L -NAME for 6 wk developed proteinuria and renal injury, whereas WF rats receiving 150 mg/l L -NAME for 6–10 wk or 300 mg/l for 6 wk developed no proteinuria and minimal renal injury. Blood pressure was significantly elevated with chronic NOSI in both strains but was higher in the SD rat. There was little impact on renal nitric oxide synthase expression with L -NAME, except that cortical endothelial nitric oxide synthase abundance increased in WF after 6 wk (150 mg/l). Micropuncture experiments with acute pressor NOSI resulted in similar increases in systemic blood pressure in SD and WF rats, whereas WF rats showed a much smaller increment in glomerular blood pressure compared with SD rats. In conclusion, WF rats do not develop renal injury after chronic NOSI at, or above, a dose that causes significant injury in the SD rat. This protection may be associated with protection from glomerular hypertension. proteinuria; glomerular sclerosis; creatinine clearance; Sprague- Dawley Address for reprint requests and other correspondence: Corresponding author: C. Baylis, Dept. of Physiology and Functional Genomics, 1600 SW Archer Rd., P. O. Box 100274, Univ. of Florida, Gainesville, FL 32610–0274 (e-mail: baylisc{at}ufl.edu )
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We previously showed that the Wistar-Furth (WF) rats are resistant to several models of CKD and maintain renal nitric oxide (NO) production compared with SD rats, whereas low-dose NOSI caused progression of CKD in WF rats. Here, we evaluate the impact of high-dose chronic NOSI in WF and SD rats, as well as intrarenal responses to an acute pressor dose of NOSI in the normal WF. Rats were given N G -nitro- L -arginine methyl ester ( L -NAME) (150 and 300 mg/l for 6–10 wk) in the drinking water after an initial bolus tail vein injection. Both strains showed significant reductions in total NO production with chronic L -NAME. SD given 150 mg/l L -NAME for 6 wk developed proteinuria and renal injury, whereas WF rats receiving 150 mg/l L -NAME for 6–10 wk or 300 mg/l for 6 wk developed no proteinuria and minimal renal injury. Blood pressure was significantly elevated with chronic NOSI in both strains but was higher in the SD rat. There was little impact on renal nitric oxide synthase expression with L -NAME, except that cortical endothelial nitric oxide synthase abundance increased in WF after 6 wk (150 mg/l). Micropuncture experiments with acute pressor NOSI resulted in similar increases in systemic blood pressure in SD and WF rats, whereas WF rats showed a much smaller increment in glomerular blood pressure compared with SD rats. In conclusion, WF rats do not develop renal injury after chronic NOSI at, or above, a dose that causes significant injury in the SD rat. This protection may be associated with protection from glomerular hypertension. proteinuria; glomerular sclerosis; creatinine clearance; Sprague- Dawley Address for reprint requests and other correspondence: Corresponding author: C. Baylis, Dept. of Physiology and Functional Genomics, 1600 SW Archer Rd., P. O. 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Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>1 Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, Pennsylvania; 2 Department of Nutrition, West Virginia University, Morgantown, West Virginia; and 3 Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida Submitted 23 June 2005 ; accepted in final form 25 August 2005 Chronic nitric oxide synthase inhibition (NOSI) causes chronic kidney disease (CKD) in the Sprague Dawley (SD) rat. We previously showed that the Wistar-Furth (WF) rats are resistant to several models of CKD and maintain renal nitric oxide (NO) production compared with SD rats, whereas low-dose NOSI caused progression of CKD in WF rats. Here, we evaluate the impact of high-dose chronic NOSI in WF and SD rats, as well as intrarenal responses to an acute pressor dose of NOSI in the normal WF. Rats were given N G -nitro- L -arginine methyl ester ( L -NAME) (150 and 300 mg/l for 6–10 wk) in the drinking water after an initial bolus tail vein injection. Both strains showed significant reductions in total NO production with chronic L -NAME. SD given 150 mg/l L -NAME for 6 wk developed proteinuria and renal injury, whereas WF rats receiving 150 mg/l L -NAME for 6–10 wk or 300 mg/l for 6 wk developed no proteinuria and minimal renal injury. Blood pressure was significantly elevated with chronic NOSI in both strains but was higher in the SD rat. There was little impact on renal nitric oxide synthase expression with L -NAME, except that cortical endothelial nitric oxide synthase abundance increased in WF after 6 wk (150 mg/l). Micropuncture experiments with acute pressor NOSI resulted in similar increases in systemic blood pressure in SD and WF rats, whereas WF rats showed a much smaller increment in glomerular blood pressure compared with SD rats. 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We previously showed that the Wistar-Furth (WF) rats are resistant to several models of CKD and maintain renal nitric oxide (NO) production compared with SD rats, whereas low-dose NOSI caused progression of CKD in WF rats. Here, we evaluate the impact of high-dose chronic NOSI in WF and SD rats, as well as intrarenal responses to an acute pressor dose of NOSI in the normal WF. Rats were given N G -nitro- L -arginine methyl ester ( L -NAME) (150 and 300 mg/l for 6–10 wk) in the drinking water after an initial bolus tail vein injection. Both strains showed significant reductions in total NO production with chronic L -NAME. SD given 150 mg/l L -NAME for 6 wk developed proteinuria and renal injury, whereas WF rats receiving 150 mg/l L -NAME for 6–10 wk or 300 mg/l for 6 wk developed no proteinuria and minimal renal injury. Blood pressure was significantly elevated with chronic NOSI in both strains but was higher in the SD rat. There was little impact on renal nitric oxide synthase expression with L -NAME, except that cortical endothelial nitric oxide synthase abundance increased in WF after 6 wk (150 mg/l). Micropuncture experiments with acute pressor NOSI resulted in similar increases in systemic blood pressure in SD and WF rats, whereas WF rats showed a much smaller increment in glomerular blood pressure compared with SD rats. In conclusion, WF rats do not develop renal injury after chronic NOSI at, or above, a dose that causes significant injury in the SD rat. This protection may be associated with protection from glomerular hypertension. proteinuria; glomerular sclerosis; creatinine clearance; Sprague- Dawley Address for reprint requests and other correspondence: Corresponding author: C. Baylis, Dept. of Physiology and Functional Genomics, 1600 SW Archer Rd., P. O. 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source American Physiological Society Journals; MEDLINE; Free E-Journal (出版社公開部分のみ)
subjects Animals
Chronic Disease
Dose-Response Relationship, Drug
Kidney - enzymology
Kidney - pathology
Kidney Diseases - chemically induced
Kidney Diseases - enzymology
Kidney Diseases - pathology
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - metabolism
Nitrogen Dioxide - urine
omega-N-Methylarginine - pharmacology
Puromycin - toxicity
Rats
Rats, Inbred WF
Rats, Sprague-Dawley
Time Factors
title Resistance to renal damage by chronic nitric oxide synthase inhibition in the Wistar-Furth rat
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