Document Detail

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle.
MedLine Citation:
PMID:  21536852     Owner:  NLM     Status:  MEDLINE    
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.
Darren P Casey; Michael J Joyner
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-05-02
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  301     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-30     Completed Date:  2011-08-30     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H261-8     Citation Subset:  IM    
Dept. of Anesthesiology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Acetylcholine / administration & dosage,  pharmacology
Blood Pressure / drug effects,  physiology
Brachial Artery / physiology
Cyclooxygenase Inhibitors / pharmacology
Enzyme Inhibitors / pharmacology
Exercise / physiology*
Forearm / blood supply,  physiology
Heart Rate / drug effects,  physiology
Hyperemia / physiopathology
Ketorolac / pharmacology
Muscle, Skeletal / blood supply,  physiology*
Nitric Oxide / physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Prostaglandins / physiology*
Regional Blood Flow / physiology
Vasodilation / drug effects,  physiology*
Vasodilator Agents / administration & dosage,  pharmacology
Vital Capacity / physiology
Young Adult
omega-N-Methylarginine / pharmacology
Grant Support
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Enzyme Inhibitors; 0/Prostaglandins; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 51-84-3/Acetylcholine; 66635-83-4/Ketorolac; EC Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Fetal programming of pulmonary vascular dysfunction in mice: role of epigenetic mechanisms.
Next Document:  sGC{alpha}1 mediates the negative inotropic effects of NO in cardiac myocytes independent of changes...