Chronic hypoxia was demonstrated to induce right ventricular hypertrophy and changes in right coronary artery blood flow. Moreover, it induced a vasodilation in the whole heart, but it is not clear whether hypoxia-mediated vasodilation occurs (Thorne et al.,2004). We hypothetized that chronic hypoxia could modify reactivity of right coronary artery myocytes by K⁺-current modulation. Seven weeks old male Wistar rats were housed in a hypoxic chamber during 3 weeks (PO2 = 75 mmHg) and were compared to normoxic rats (PO2 = 150 mmHg). Animals were killed by pentobarbital injection (60 mg.kg^-1 ip). The descending anterior branch of the left coronary artery and the main branch of the right coronary artery were dissected. Coronary artery myocytes were isolated by enzymatic digestion as previously described (Barbe et al.,2002). Outward currents were recorded using Patch-Clamp technique. They were generated by membrane depolarization pulse of 8 mV (400 ms) from a holding potential of -60 mV and up to +60 mV. Results are expressed as mean±S.E.M., n represents the number of cells. Outward current-density in right coronary artery (RCA n=22) myocytes was higher than in left coronary artery (LCA n=15) myocytes (21.3±2.6 pA/pF vs 14.9±3.1 pA/pF). Moreover RCA myocytes were less depolarized than LCA myocytes (-24.8±1.2 mV vs -20.6±1.2 mV). Chronic hypoxia induced a decrease in outward current-density in RCA myocytes (13.9±1.1 pA/pF n=14) and it depolarized the cell membrane (-17.7±1.9 mV). In opposite, chronic hypoxia increased outward current-density in LCA myocytes (27.5±4.7 pA/pF n=8) and hyperpolarized the cell membrane (-25.0±1.9 pA/pF). To further characterise the hypoxic-sensitive current, we used 4-AP, a well known blocker of voltage-gated K+-channels. The 4-AP-sensitive current was significantly lower in LCA (n=7) compared to RCA (n=12) myocytes (4.8±2.3 pA/pF vs 9.6±2.6 pA/pF). We found that chronic hypoxia decreased the 4-AP-sensitive current in RCA myocytes (4.5±0.9 pA/pF n=8) but it increased the 4-AP-sensitive current in LCA myocytes (11.5±5.1 pA/pF n=3). We conclude that chronic hypoxia has opposite effects on 4-AP-sensitive current on right and left coronary myocytes. Whilst this current was decreased in RCA myocytes it was increased in LCA myocytes. This difference is probably linked to a differential expression of Kv-channels sensitive to hypoxia in LCA and RCA myocytes. Identity of these channels remains to be discovered.