Impact of combined NO and PG blockade on rapid vasodilation in a forearm mild-to-moderate exercise transition in humans

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Abstract
We tested the hypothesis that nitric oxide (NO) and prostaglandins (PGs) contribute to the rapid vasodilation that accompanies a transition from mild to moderate exercise. Nine healthy volunteers (2 women and 7 men) lay supine with forearm at heart level. Subjects were instrumented for continuous brachial artery infusion of saline (control condition) or combined infusion of NG-nitro-l-arginine methyl ester (l-NAME) and ketorolac (drug condition) to inhibit NO synthase and cyclooxygenase, respectively. A step increase from 5 min of steady-state mild (5.4 kg) rhythmic, dynamic forearm handgrip exercise (1 s of contraction followed by 2 s of relaxation) to moderate (10.9 kg) exercise for 30 s was performed. Steady-state forearm blood flow (FBF; Doppler ultrasound) and forearm vascular conductance (FVC) were attenuated in drug compared with saline (control) treatment: FBF = 196.8 ± 30.8 vs. 281.4 ± 34.3 ml/min and FVC = 179.3 ± 29.4 vs. 277.8 ± 34.8 ml·min−1·100 mmHg−1 (both P < 0.01). FBF and FVC increased from steady state after release of the initial contraction at the higher workload in saline and drug conditions: ΔFBF = 72.4 ± 8.7 and 52.9 ± 7.8 ml/min, respectively, and ΔFVC = 66.3 ± 7.3 and 44.1 ± 7.0 ml·min−1·100 mmHg−1, respectively (all P < 0.05). The percent ΔFBF and ΔFVC were not different during saline infusion or combined inhibition of NO and PGs: ΔFBF = 27.2 ± 3.1 and 28.1 ± 3.8%, respectively ( P = 0.78) and ΔFVC = 25.7 ± 3.2 and 26.0 ± 4.0%, respectively ( P = 0.94). The data suggest that NO and vasodilatory PGs are not obligatory for rapid vasodilation at the onset of a step increase from mild- to moderate-intensity forearm exercise. Additional vasodilatory mechanisms not dependent on NO and PG release contribute to the immediate and early increase in blood flow in an exercise-to-exercise transition.