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Background: Diabetes decreased cardioprotective potential of ischemic postconditioning (IPOC), atrial natriuretic peptide (ANP) induced the cardioprotection against ischemic-reperfusion (I/R) injury. The present study has been designed to investigate the role of ANP induced postconditioning in diabetic rat heart. Methods: Isolated Langendorff perfused normal and diabetic rat hearts were stabilized for 10 min proceed by global ischemia further followed by four cycles of IPOC, each cycle comprised 5 min of reperfusion and 5 min of ischemia at onset of 120 min of reperfusion. Perfusion of ANP (0.1μM/l) with Krebs–Henseleit Buffer solution in isolated diabetic rat heart for four-cycle of IPOC significantly decreased I/R-induced myocardial infarct size and release of CK-MB and lactate dehydrogenase (LDH) level in coronary effluent. Results: Four cycles of IPOC-induced cardioprotection noted by decreased in infarct size and also in release of LDH and CK-MB in normal rat heart. However, IPOC-induced cardioprotection was completely attenuated in isolated heart obtained from diabetic rat. Perfusion of ANP (0.1μM/L) significantly restored the attenuated cardioprotection in diabetic rat heart, which was completely blocked by perfusion of L-NAME (100μM/L), an eNOS inhibitor. Conclusion: So that, ANP restored cardioprotective affect in diabetic rat heart, which was completely abolished by the perfusion of L-NAME (100μM/L), an eNOS inhibitor.