Objective: Experimental and clinical studies indicate that cardiovascular system diseases have the highest mortality rate. One of the major factors underlying this high mortality rate is hypoxia. The inward rectifying potassium channel 6.2 (Kir6.2) plays a key role in the adaptation and metabolic regulation of cardiac tissue to hypoxia. In this study, the effect of chloroquine on Kir6.2 expression in heart tissue exposed to moderate chronic hypoxia was investigated. Methods: In this study, 32 8-12-week-old male Wistar albino rats weighing 200-300 g were used in 4 groups. Accordingly, the first group exposed to a normoxic (at 21% O 2 concentration) environment, the second group was administered daily chloroquine (50 mg/kg intraperitoneal) injection in a normoxic environment, the third group exposed to a moderately hypoxic environment (10% O2 concentration), and the fourth group in the hypoxic environment had chloroquine (50 mg/kg intraperitoneal) injection. At the end of the 28-day period, the heart tissues were dissected with anesthesia. Immunohistochemical analysis was performed for Kir6.2 channels. Results: In hypoxic heart tissue, a significant decrease in Kir6.2 immunoreactivity was observed due to chloroquine administration compared to the control group (p<0.05). In addition, in the hypoxia group, which was also treated with chloroquine, hemorrhagic areas were significantly reduced compared to the control group (p<0.001). Conclusion: Data may demonstrate the potential protective and adaptive effects of chloroquine in hypoxic heart. Further molecular and functional studies are required to confirm the Kir6.2 related mechanism.