Key result
Chronic NO synthesis inhibition with L-NAME exacerbated cyclosporin-induced increases in arterial pressure and renal resistances, suggesting NO synthesis counterbalances preglomerular vasoconstriction.
Why the study?
Does NO synthesis inhibition exacerbate cyclosporin nephrotoxicity in uninephrectomized rats?
Population
Uninephrectomized rats
Comparison
Cyclosporin A 30 mg/kg + nitro-L-arginine methyl… vs Vehicle (Veh), CsA alone, and Veh + L-NAME
Design
Preclinical
Follow-up
7 days
Authors
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Should not alter cyclosporin use in patients; hypothesis-generating for NO-targeted renoprotection pending clinical trials.
Does NO synthesis inhibition exacerbate cyclosporin nephrotoxicity in uninephrectomized rats?
NO synthesis, likely driven by increased eNOS mRNA expression, is enhanced at the cortical level during cyclosporin nephrotoxicity to counterbalance preglomerular vasoconstriction.
Bobadilla et al. (1998) studied Cyclosporin nephrotoxicity. Cyclosporin A + nitro-L-arginine methyl ester (L-NAME) vs. Vehicle, CsA alone, and Vehicle + L-NAME was evaluated on Glomerular hemodynamic and histological changes, and NO synthases mRNA expression. Chronic NO synthesis inhibition with L-NAME exacerbated cyclosporin-induced increases in arterial pressure and renal resistances, suggesting NO synthesis counterbalances preglomerular vasoconstriction.
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