Participation of ATP dependent K channels to the renal ischemia injury under the effect of erytropoietin: HIF-1 mRNA expression changes

Erytropoietin (EPO) is a protective cytokine which is secreted against hypoxia. Receptors of EPO is found in many tissues. Protective effects of EPO were showed in different ıschemia reperfusion (I/R) cell or tissue models. Potassium (K) channel openers act as ischemic preconditioning like effect in I/R. In I/R ınjury hypoxia inducable factor (HIF) is activated. Because of the common pathways of EPO and K channel, we aimed to study the effects of EPO and K channel inhibitors (glibenclamid) of openers (diazoxide) in I/R.Under normal and hypoxic conditions, EPO, diazoxide, glibenclamid were used in kidney proximal tubule cell culture. Cell groups cmposed of EPO with doses of 1, 5, 10, 50 iu/ml, diazoxide with doses of 10, 100 ?M, glibenclamid with doses of 10, 100 ?M and both EPO and glibenclamid. Cell proliferation, apoptosis and HIF mRNA expression were evaluated by MTT, Kaspaz-3 and polymerase chain reaction (PCR) respectively. Results were evaluated by oneway ANOVA testProliferative effect was seen with EPO, decreased cell was seen in glibenclamid usage (p<0.001). Usage of EPO and glibenclamid together slightly corrected the decreased cell number occured by glibenclamid. EPO was protective in hypoxia. Diazoxide is also protective for hypoxic cell death (p<0.001There is a significant role of K channels in the protective effects of EPO for I/R. Usage of EPO is inhibiting the detrimental effects of glibenclamid. For this reason usage of EPO and avoidance of K channel blockers in renal transplantation may be useful.