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

Darren P. Casey, Michael J. Joyner

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


We tested thehypothesis that 1) prostaglandins (PGs) contribute to compensatoryvasodilation in contracting human forearm subjected to acute hypoperfusion,and 2) the combined inhibition of PGs and nitric oxidewould attenuate the compensatory vasodilation more than PG inhibitionalone. In separate protocols, subjects performed forearm exercise(20% of maximum) during hypoperfusion evoked by intra-arterialballoon inflation. Each trial included baseline, exercise before inflation,exercise with inflation, and exercise after deflation. Forearmblood flow (FBF; ultrasound) and local (brachial artery) and systemicarterial pressure [mean arterial pressure (MAP); Finometer] weremeasured. In protocol 1 (n = 8), exercise was repeated duringcyclooxygenase (COX) inhibition (Ketorolac) alone and during Ketorolac-NOS inhibition [NG-monomethyl-L-arginine (L-NMMA)]. Inprotocol 2 (n = 8), exercise was repeated during L-NMMA alone andduring L-NMMA-Ketorolac. Forearm vascular conductance (FVC;ml·min-1 ·100 mmHg-1) was calculated from FBF (ml/min) andlocal MAP (mmHg). The percent recovery in FVC during inflationwas 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 comparedwith the control (no drug) trial (92 ± 11 vs. 100 ± 10%, P = 0.83).However, combined COX-nitric oxide synthase (NOS) inhibitioncaused a substantial reduction in %FVC recovery (54 ± 8%, P < 0.05vs. Ketorolac alone). In protocol 2, the percent recovery in FVC wasattenuated 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 thatPGs are not obligatory to the compensatory dilation observed duringforearm exercise with hypoperfusion.

Original languageEnglish (US)
Pages (from-to)H261-H268
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1
StatePublished - Jul 2011


  • Blood flow
  • Exercise
  • Hypoperfusion
  • Nitric oxide
  • Prostaglandins
  • Vasodilation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


Dive into the research topics of 'Prostaglandins do not contribute to the nitric oxide-mediated compensatoryvasodilation in hypoperfused exercising muscle'. Together they form a unique fingerprint.

Cite this