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Hyperhomocysteinemia induces renal hemodynamic dysfunction: is nitric oxide involved?
Patricia A Fischer1, Graciela N Dominguez, Luis A Cuniberti
1Section of Pharmacology, Department of Physiology, Favaloro University, Buenos Aires, Argentina.
Journal of the American Society of Nephrology : JASN
|February 22, 2003
Summary
Hyperhomocysteinemia causes renal oxidative stress and dysfunction by impairing nitric oxide (NO) pathways. This study in rats shows reduced NO bioavailability and increased sensitivity to NO inhibition, leading to kidney damage.
Area of Science:
- Nephrology
- Cardiovascular Research
- Biochemistry
Background:
- Hyperhomocysteinemia is linked to endothelial dysfunction, but the mechanisms are unclear.
- Nitric oxide (NO) is crucial for regulating systemic and renal hemodynamics.
Purpose of the Study:
- To investigate if hyperhomocysteinemia induces renal oxidative stress and dysfunction.
- To determine the role of the NO-pathway in hyperhomocysteinemia-induced renal impairment.
Main Methods:
- Wistar rats were divided into control and hyperhomocysteinemic groups for 8 weeks.
- Measured plasma homocysteine, renal oxidative stress markers (superoxide anion, nitrotyrosine), nitrite+nitrate levels, and renal function (GFR, RPF, RVR).
- Assessed NO pathway involvement using L-Arginine and L-NAME challenges.
Main Results:
- Hyperhomocysteinemic rats exhibited elevated homocysteine, superoxide anion production, nitrotyrosine, and nitrite+nitrate levels.
- Renal function was impaired in hyperhomocysteinemic rats, with lower GFR and RPF, and higher RVR.
- Responses to L-Arginine and L-NAME indicated reduced NO bioavailability and enhanced sensitivity to NO inhibition.
Conclusions:
- Hyperhomocysteinemia induces significant oxidative stress in the kidneys.
- NO inactivation and disturbances in the NO-pathway contribute to renal dysfunction in hyperhomocysteinemia.
- These findings highlight the detrimental effects of elevated homocysteine on renal health.