TY - JOUR
T1 - Roles of nitric oxide and prostaglandins in the hyperemic response to a maximal metabolic stimulus
T2 - Redundancy prevails
AU - Lopez, Marcos G.
AU - Silva, Bruno M.
AU - Joyner, Michael J.
AU - Casey, Darren P.
N1 - Funding Information:
Acknowledgments We would like to acknowledge Drs. Tim Curry and John Eisenach for their instrumental role in making these experiments possible. Also, we would like to thank Branton Walker, Chris Johnson, Alex Allen, John Roger Shepherd, and Alex White for technical assistance, and Pamela Engrav for her aid in recruiting research participants. This publication was made possible by National Institutes of Health grants HL46493 (M.J.J.), AR-55819 (D.P.C.) and CTSA RR-024150. The Caywood Professorship via the Mayo Foundation also supported this research. We also acknowledge stipend support from Brazil’s Coordination for the Improvement of Higher Education Personnel (CAPES).
PY - 2013/6
Y1 - 2013/6
N2 - 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.
AB - 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.
KW - Hyperemia
KW - Ischemia
KW - Nitric oxide
KW - Prostaglandins
KW - Vasodilation
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U2 - 10.1007/s00421-012-2570-y
DO - 10.1007/s00421-012-2570-y
M3 - Article
C2 - 23250568
AN - SCOPUS:84878242721
SN - 1439-6319
VL - 113
SP - 1449
EP - 1456
JO - European Journal of Applied Physiology
JF - European Journal of Applied Physiology
IS - 6
ER -