Abstract
We examined carbon monoxide (CO) delivery by carbon monoxide‐releasing molecule 2 (CORM‐2) or hemoglobin (Hb) on cellular oxygen sensing and mitochondrial respiration in bovine aortic endothelial cells (BAECs). CORM‐2 reduced hypoxia‐inducible factor‐1α (HIF‐1α) and endothelin‐1 (ET‐1) expression in normoxic and hypoxic cells, but while Hb alone significantly reduced HIF‐1α stabilization in hypoxic cells, CO delivered by Hb (Hb‐CO) had no effect on HIF‐1α stabilization. CO dose‐dependently increased basal oxygen consumption and reduced overall mitochondrial respiratory capacity. Hb‐CO increased basal oxygen consumption but did not alter respiratory capacity. Together, CO reduced ET‐1, and, at low doses, had no effect on endothelial mitochondria oxygen consumption. CO ligation to Hb may be developed further as non‐vasoactive oxygen therapeutic without compromising mitochondrial function.