ArticleThe Korean journal of internal medicine1999
Role of nitric oxide in the pathogenesis of diabetic nephropathy in streptozotocin-induced diabetic rats.
Article in The Korean journal of internal medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 44 citations in OpenAlex.
- Glucose and Blood Pressure-Dependent Pathways-The Progression of Diabetic Kidney Disease.International journal of molecular sciences · 2020Review
- Antioxidant, α-Amylase and α-Glucosidase Inhibitory Activities and Potential Constituents ofMolecules (Basel, Switzerland) · 2019Article
- Salt sensitivity of nitric oxide generation and blood pressure in mice with targeted knockout of the insulin receptor from the renal tubule.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- The kallikrein-kinin system in diabetic nephropathy.Kidney international · 2012Review
- The role of nitric oxide in the dysregulation of the urine concentration mechanism in diabetes mellitus.Frontiers in physiology · 2012Article
- Continuously measured renal blood flow does not increase in diabetes if nitric oxide synthesis is blocked.American journal of physiology. Renal physiology · 2008Article
- Role of glomerular filtration rate in controlling blood pressure early in diabetes.Hypertension (Dallas, Tex. : 1979) · 2008Review
- Posttranslational regulation of NO synthase activity in the renal medulla of diabetic rats.American journal of physiology. Renal physiology · 2005Article
- Autocrine and paracrine mechanisms in the early stages of diabetic nephropathy.Journal of endocrinological investigation · 1999Review
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectivesSeveral reports suggest that enhanced generation or actions of nitric oxide (NO) have been implicated in the pathogenesis of glomerular hyperfiltration and hyperperfusion that occurs in early diabetes. However, the precise role of altered NO generation in the pathogenesis of diabetic nephropathy is unclear. The present study was aimed at investigating the role of nitric oxide in the pathogenesis of glomerular hyperfiltration and hyperperfusion in streptozotocin-induced diabetic rats.
methodsTo evaluate the role of NO in diabetic hyperfiltration, we measured plasma and urine concentrations of NO2-/NO3-, stable metabolic products of NO and protein expressions of three isoforms of nitric oxide synthase (NOS) in streptozotocin-induced diabetic rats. We also investigated renal hemodynamic changes, such as glomerular filtration rate (GFR) and renal plasma flow (RPF), in responses to acute and chronic administration of NO synthesis inhibitor, nitro-L-arginine methyl ester (L-NAME), in diabetic and control rats.
resultsDiabetic rats exhibited significantly elevated plasma and urinary NO2-/NO3- levels at 28 days after streptozotocin injection, and total excretion of NO2-/NO3- was approximately five-fold higher in diabetic rats than controls. Insulin and L-NAME treatment prevented the increases in plasma and urinary NO2-/NO3- concentrations in diabetic rats, respectively. The three isoforms of NOS (bNOS, iNOS, and ecNOS) were all increased in the renal cortex, whereas they remained unaltered in the renal medulla at day 28. GFR and RPF were significantly elevated in diabetic rats, and acute and chronic inhibition of NO synthesis by L-NAME attenuated the renal hemodynamic changes (increases in GFR and RPF) in diabetic rats, respectively.
conclusionsNO synthesis was increased due to enhanced NOS expression in diabetic rats, and chronic NO blockade attenuated renal hyperfiltration and hyperperfusion in diabetic rats. In addition, diabetic rats exhibited enhanced renal hemodynamic responses to acute NO inhibition and excreted increased urinary NO2-/NO3-. These results suggest that excessive NO production may contribute to renal hyperfiltration and hyperperfusion in early diabetes.
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