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Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle
Journal article   Open access   Peer reviewed

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Darren P Casey and Michael J Joyner
American journal of physiology. Heart and circulatory physiology, Vol.301(1), pp.H261-268
07/2011
DOI: 10.1152/ajpheart.00222.2011
PMCID: PMC3129921
PMID: 21536852
url
https://doi.org/10.1152/ajpheart.00222.2011View
Published (Version of record) Open Access

Abstract

We tested the hypothesis that 1) prostaglandins (PGs) contribute to compensatory vasodilation in contracting human forearm subjected to acute hypoperfusion, and 2) the combined inhibition of PGs and nitric oxide would attenuate the compensatory vasodilation more than PG inhibition alone. In separate protocols, subjects performed forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included baseline, exercise before inflation, exercise with inflation, and exercise after deflation. Forearm blood flow (FBF; ultrasound) and local (brachial artery) and systemic arterial pressure [mean arterial pressure (MAP); Finometer] were measured. In protocol 1 (n = 8), exercise was repeated during cyclooxygenase (COX) inhibition (Ketorolac) alone and during Ketorolac-NOS inhibition [N(G)-monomethyl-l-arginine (l-NMMA)]. In protocol 2 (n = 8), exercise was repeated during l-NMMA alone and during l-NMMA-Ketorolac. Forearm vascular conductance (FVC; ml·min(-1)·100 mmHg(-1)) was calculated from FBF (ml/min) and local MAP (mmHg). The percent recovery in FVC during inflation was calculated as (steady-state inflation + exercise value - nadir)/[steady-state exercise (control) value - nadir] × 100. In protocol 1, COX inhibition alone did not reduce the %FVC recovery compared with the control (no drug) trial (92 ± 11 vs. 100 ± 10%, P = 0.83). However, combined COX-nitric oxide synthase (NOS) inhibition caused a substantial reduction in %FVC recovery (54 ± 8%, P < 0.05 vs. Ketorolac alone). In protocol 2, the percent recovery in FVC was attenuated with NOS inhibition alone (69 ± 9 vs. 107 ± 10%, P < 0.01) but not attenuated further during combined NOS-COX inhibition (62 ± 10%, P = 0.74 vs. l-NMMA alone). Our data indicate that PGs are not obligatory to the compensatory dilation observed during forearm exercise with hypoperfusion.
 Humans Nitric Oxide Synthase - antagonists & inhibitors Male omega-N-Methylarginine - pharmacology Young Adult Heart Rate - drug effects Forearm - blood supply Heart Rate - physiology Blood Pressure - drug effects Blood Pressure - physiology Forearm - physiology Vasodilation - physiology Muscle, Skeletal - blood supply Vasodilator Agents - pharmacology Catheterization Acetylcholine - pharmacology Enzyme Inhibitors - pharmacology Nitric Oxide - physiology Muscle, Skeletal - physiology Cyclooxygenase Inhibitors - pharmacology Acetylcholine - administration & dosage Prostaglandins - physiology Hyperemia - physiopathology Vital Capacity - physiology Exercise - physiology Vasodilation - drug effects Regional Blood Flow - physiology Ketorolac - pharmacology Vasodilator Agents - administration & dosage Brachial Artery - physiology

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