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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
Renal dysfunction after chronic blockade of nitric oxide synthesis
Victoria Cachofeiro1, Lourdes A Fortepiani, Josefa Navarro-Cid
1Departamentos de Fisiología, Facultades de Medicina, Universidad Complutense de Madrid, Spain. vcara@med.ucm.es
Antioxidants & Redox Signaling
|February 8, 2003
Summary
Chronic inhibition of nitric oxide (NO) impaired kidney function and caused renal damage in rats. This highlights NO's crucial renoprotective role and suggests sympathoadrenal system activation contributes to these effects.
Area of Science:
- Nephrology
- Physiology
- Pharmacology
Background:
- Nitric oxide (NO) plays a vital role in regulating renal hemodynamics and tubular function.
- Understanding the consequences of chronic NO inhibition is crucial for renal health research.
Purpose of the Study:
- To investigate the long-term effects of nitric oxide synthesis inhibition on rat renal function.
- To evaluate the impact of L-NAME on various vasoactive systems and renal hemodynamics.
Main Methods:
- Rats were treated with N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthesis inhibitor, for 8 weeks.
- Measurements included blood pressure, glomerular filtration rate, renal blood flow, and urinary protein excretion.
- Plasma and urinary levels of vasoactive substances (renin, aldosterone, catecholamines, endothelin, thromboxane B2) were assessed.
Main Results:
- Chronic L-NAME administration significantly increased blood pressure and proteinuria.
- Glomerular filtration rate and renal blood flow were markedly reduced.
- Elevated plasma epinephrine and norepinephrine levels were observed, while renin-angiotensin system, aldosterone, endothelin, and thromboxane A2 showed no significant changes.
Conclusions:
- Chronic blockade of nitric oxide leads to significant renal dysfunction and damage in rats.
- Nitric oxide plays a critical renoprotective role.
- Activation of the sympathoadrenal system may contribute to the observed renal alterations.
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