Fig. 4.

Proposed mechanisms for hypoxia-induced vasodilation at rest and during exercise. During hypoxic exercise, nitric oxide (NO) is the final common pathway for the compensatory dilator response. Systemic epinephrine (E) release, acting via β-adrenergic receptors, contributes to the NO-mediated vasodilation at lower exercise intensities, but this β-adrenergic contribution decreases with increasing exercise intensity. ATP released from the red blood cell (RBC) and/or endothelial-derived prostacyclin (PGI₂) remain attractive candidates for stimulating NO during higher intensity hypoxic exercise. Neuronal NOS and nitrate are also potential sources of NO generation and might be another contributor to compensatory vasodilation during hypoxic exercise. Adenosine receptor (ADO-R) activation does not appear to be a major source of NO production during hypoxic exercise. α₁AR, α₂AR, and β₂AR: α₁-, α₂-, and β₂-adrenergic receptors, respectively; NE, norepinephrine; PR, purinergic receptor; SNO-Hb, S-nitrosohemoglobin.