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Hypoxic Vasodilation in Human Skeletal Muscle: contributions of nitric oxide and vasodilating prostaglandins

We tested the hypothesis that nitric oxide (NO) and prostaglandins (PGs) contribute independently to hypoxic vasodilation, and that combined inhibition would reveal a potential compensatory interaction between these two dilators in the regulation of vascular tone. In 12 healthy adults, we measured forearm blood flow (Doppler ultrasound) and calculated forearm vascular conductance (FVC) responses to 5 minutes of steady‐state isocapnic hypoxia (O2 saturation ∼85%). All trials were performed during α‐ and β‐adrenergic blockade (via brachial artery catheter) to eliminate sympathoadrenal influences on vascular tone. Hypoxic vasodilator responses were determined under control conditions, during independent NO synthase (NOS; L‐NAME) or cyclooxygenase inhibition (COX; ketorolac), and finally during combined NOS and COX inhibition. Drug order was counterbalanced across subjects. In both groups, acute hypoxia caused significant forearm vasodilation under control conditions (ΔFVC ∼25%; P<0.05), and this was not influenced by prior inhibition of NO or PGs. In contrast, combined inhibition of NO and PGs in both groups reduced hypoxic vasodilation by ∼90%. Our findings indicate that NO and PGs are not independently obligatory for regulating vascular tone during hypoxia, but that together they play a significant role in hypoxic vasodilation in human skeletal muscle.