Roles of nitric oxide and prostaglandins in the hyperemic response to a maximal metabolic stimulus: redundancy prevails

• Published in: European journal of applied physiology Vol. 113; no. 6; pp. 1449 - 1456
• Main Authors: Lopez, Marcos G., Silva, Bruno M., Joyner, Michael J., Casey, Darren P.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01.06.2013; Springer Nature B.V
• Subjects: Adenosine; Anesthesiology; Biomedical and Life Sciences; Biomedicine; Blood Pressure; Catheters; Enzyme Inhibitors - pharmacology; Exercise - physiology; Female; Forearm - blood supply; Hand Strength; Human Physiology; Humans; Hyperemia - metabolism; Ischemia; Ischemia - metabolism; Ketorolac - pharmacology; Male; Metabolism; Musculoskeletal system; Nitric oxide; Nitric Oxide - metabolism; Occupational Medicine/Industrial Medicine; omega-N-Methylarginine - pharmacology; Original Article; Prostaglandins - metabolism; Regional Blood Flow - drug effects; Regional Blood Flow - physiology; Sports Medicine; Young Adult; United States > US; Prostaglandins; Hyperemia; Ischemia; Nitric oxide; Vasodilation
• ISSN: 1439-6319; 1439-6327; 1439-6327
• DOI: 10.1007/s00421-012-2570-y

Vasodilatory mechanisms controlling post-exercise or post-ischemic hyperemia are thought to be under redundant control and remain incompletely understood. A maximal metabolic stimulus evoked by ischemic exercise (IE) might limit redundancy by full activation of multiple pathways. We tested whether nitric oxide (NO) and/or prostaglandins contribute to the hyperemic response to IE. 17 subjects were randomized into two groups and performed three trials of IE during control (saline), N G -monomethyl- l -arginine ( l -NMMA; NOS inhibition) (protocol 1) or ketorolac (cyclooxygenase inhibition) infusion (protocol 2), and combined l -NMMA/ketorolac infusion via a brachial arterial catheter. Forearm blood flow (FBF) was measured with venous occlusion plethysmography following IE trials consisting of 5 min of ischemia and simultaneous rhythmic handgrip exercise (final 2 min). Peak and total (area under the curve) FBF and blood pressure (MAP) were measured for 3 min after each trial. Forearm vascular conductance (FVC) was calculated as FBF/MAP. Change (Δ) in peak FBF and FVC from baseline differed only between peak FBF for the saline and l -NMMA + ketorolac trials in protocol 1. Peak ΔFBF was 26.8 ± 2.5, 30.0 ± 2.8, and 33.9 ± 3.6 ml 100 ml −1  min −1 for saline, l -NMMA, and l -NMMA + ketorolac trials ( P  = 0.04). For protocol 1 ( n  = 8), total ΔFVC was 59.6 ± 4.3, 57.8 ± 6.0, and 59.9 ± 5.6 ml 100 ml −1  100 mmHg −1 for saline, l -NMMA, and l -NMMA + ketorolac trials, ( P  = 0.82). For protocol 2 ( n  = 9), total ΔFVC was 54.2 ± 5.0, 56.9 ± 4.5, and 56.5 ± 5.3 ml 100 ml −1  100 mmHg −1 for saline, ketorolac, and ketorolac +  l -NMMA trials, ( P  = 0.69). These results suggest that NO and PGs are not obligatory for the hyperemic response to IE, and other vasodilator mechanisms predominate.