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Gentamicin treatment increases mesangial cell nitric oxide production
L Rivas-Cabañero1, A M Rodríguez-López, C Martínez-Salgado
1Instituto Reina Sofia de Investigacion, Nefrologica Departamento de Fisiologia y Farmacologia, Universidad de Salamanca, Spain.
Experimental Nephrology
|January 1, 1997
Summary
Gentamicin causes kidney injury by affecting mesangial cells. Endogenous nitric oxide (NO) release modulates these gentamicin-induced proliferative and contractile effects on kidney cells.
Area of Science:
- Nephrology
- Cell Biology
- Pharmacology
Background:
- Gentamicin can decrease glomerular filtration rate, potentially via mesangial cell contraction.
- The role of endogenous nitric oxide (NO) in gentamicin's effects on mesangial cells is not fully understood.
Purpose of the Study:
- To investigate the role of endogenous nitric oxide (NO) in modulating gentamicin's effects on mesangial cell proliferation and contraction.
Main Methods:
- Assessed NO synthesis via nitrite production and measured inducible nitric oxide synthase (iNOS) mRNA expression.
- Evaluated mesangial cell contraction and proliferation using cell surface area measurements and [3H]thymidine incorporation.
- Utilized L-NAME (a nitric oxide synthase inhibitor) and L-arginine (a nitric oxide precursor) for modulatory studies.
Main Results:
- Gentamicin increased NO synthesis and iNOS expression in mesangial cells.
- Gentamicin induced mesangial cell contraction and proliferation.
- L-arginine significantly attenuated gentamicin's contractile and proliferative effects, while L-NAME blocked the increase in NO synthesis.
Conclusions:
- Gentamicin induces mesangial cell contraction and proliferation, partly mediated by iNOS expression and NO release.
- Endogenous NO synthesis plays a modulatory role in gentamicin's nephrotoxic effects on mesangial cells.
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