The Effect of K-ATP Channel Blockage During Erythropoietin Treatment in Renal Ischemia-Reperfusion Injury

Abstract

ATP dependent K channels (K-ATP) take part in the Erythropoietin (EPO) induced cardioprotection but these channel activations have role in cytoprotective role of EPO in the renal ischemia reperfusion (IR) damage is still unknown. For this purpose rats were pretreated with EPO (500 IU/kg) and/or K-ATP channel blocker glibenclamide (40mM/kg) i.p. before bilateral renal IR damage. Renal tissues were used for histological examination and measurement of caspase-3 and TNF-α levels. Renal functions were evaluated by glomerular filtration rate (GFR) fractional excretion of sodium (FENa) and potassium (FEK). Renal TNF-α and caspase-3 levels were decreased in both glibenclamide and EPO-treated IR rats compared to untreated rats. The protection afforded by the pretreatment with EPO alone was greater than that of administering glibenclamide alone. Application of glibenclamide at the same time partly abolished the cytoprotective effect of EPO treatment. K-ATP mediated cytoprotection is not the main mechanism of protective effect of EPO.

KEYWORDS:

• erythropoietin (EPO)
• renal ischemia reperfusion (IR) injury
• glibenclamide
• ATP dependent K channels
• glomerular filtration rate (GFR)
• fractional sodium excretion
• (FeNa)
• fractional potassium excretion (FeK)
• caspase-3
• TNF-α