Renal
ischemia/reperfusion (I/R) injury is a common pathological condition. Studies reported renal toxicity following administration of
triptans, which are commonly used for treating
migraine headaches. To investigate the effects of
sumatriptan and the molecular mechanisms involved in renal I/R injury in rats,
ischemia was induced by bilateral clamping of renal pedicles followed by 24 h of reperfusion.
Sumatriptan was administered in three different doses (5, 10, and 20 mg/kg) before I/R injury induction. Biochemical and histopathological changes were evaluated. The contribution of
nitric oxide in modulating the effects of
sumatriptan was determined by administrating
aminoguanidine at 50 mg/kg 60 min before I/R injury. The tissue level of
nitrite,
superoxide dismutase (SOD), and
malondialdehyde (MDA) were measured.
Sumatriptan at 10 and 20 mg/kg increased the serum level of
creatinine (Cr) and blood
urea nitrogen (BUN) significantly. There was also a significant increase in
nitrite level of animals that received 10 mg/kg
sumatriptan. Co-administration of
sumatriptan with
aminoguanidine significantly decreased the BUN and Cr. Depletion of SOD level (P < 0.05) and elevation of serum levels of MDA (P < 0.001) indicated the involvement of oxidative stress in
sumatriptan adverse effects. Overall, the administration of
sumatriptan intensified renal I/R injury through activation of
inducible nitric oxide synthase and oxidative responses in rats.