Protective effects of limb remote ischemic per-conditioning on the heart injury induced by renal ischemic-reperfusion through the interaction of the apelin with the RAS/iNOS pathway

Introduction: Remote ischemic conditioning upregulates endogenous protective pathways in response to ischemia-reperfusion injury. This study tested the hypothesis that limb remote per-conditioning (RIPerC) exerts cardioprotective effects via renin-angiotensin system (RAS)/inducible nitric oxide synthase (iNOS)/apelin pathway. Methods: Renal injury (I/R) was induced by bilateral occlusion of renal pellicles for 60 minutes, followed 24 hours reperfusion; sham-operated rats served as controls. RIPerC four cycles (5 minutes) along with ischemia. The functional disturbance evaluated (BUN and creatinine) cardiac (troponin I lactate dehydrogenase) biomarkers. Results: I/R increased biomarkers were reduced group. Histopathological findings kidney heart also suggestive amelioration injury-induced changes Assessment electrophysiology revealed ameliorated decline P wave duration without significantly affecting other electrophysiological changes. Further, plasma (322.40±34.01 IU/L), (8.27±1.10 mIU/mg Protein), (68.28±10.28 Protein) angiotensin-converting enzyme (ACE) activities association elevations urine nitrite (25.47±2.01 & 16.62±3.05 μmol/L) nitrate (15.47±1.33 5.01±0.96 levels; these reversed RIPerC. (P=0.047) decreased (but not cardiac) apelin mRNA expression, while ACE2 (P<0.05) iNOS (P=0.043) expressions compared sham group; largely Conclusion: Our results indicated protects against injury, likely interaction RAS/iNOS