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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
Reduction in basal nitric oxide activity causes albuminuria
Christian Ott1, Markus P Schneider, Christian Delles
1Department of Nephrology and Hypertension, University of Erlangen-Nürnberg, Erlangen, Germany.
Diabetes
|January 29, 2011
Summary
Nitric oxide (NO) synthase inhibition increases albuminuria in patients with type 2 diabetes and hypercholesterolemia. This albuminuria increase is independent of blood pressure changes, highlighting NO
Area of Science:
- Nephrology
- Cardiovascular Research
- Endocrinology
Background:
- Albuminuria indicates glomerular filter malfunction.
- Endothelial nitric-oxide (NO) synthase dysfunction is linked to albuminuria in animal models.
- The role of NO in human glomerular barrier function requires further elucidation.
Purpose of the Study:
- To investigate the significance of NO for glomerular barrier function in humans.
- To analyze the impact of endothelial dysfunction on albuminuria.
Main Methods:
- Systemic infusion of N(G)-monomethyl-L-arginine (L-NMMA) to block NO synthases (NOSs).
- Measurement of urine albumin-to-creatinine ratio (UACR) before and after L-NMMA infusion.
- Study populations included hypertensive patients with type 2 diabetes (A) and patients with hypercholesterolemia (B).
Main Results:
- NOS inhibition with L-NMMA significantly increased UACR in both study populations.
- The increase in UACR was not correlated with changes in mean arterial pressure.
- These findings held true even after adjusting for filtration fraction.
Conclusions:
- NO synthase inhibition provokes albuminuria in humans.
- This albuminuria increase is independent of blood pressure fluctuations.
- Reduced NO activity acutely impairs endothelial function, leading to increased albuminuria, particularly in susceptible patient groups.
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