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

Darren P. Casey, Michael Joseph Joyner

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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 [N G-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)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume301
Issue number1
DOIs
StatePublished - Jul 2011

Fingerprint

Ketorolac
omega-N-Methylarginine
Economic Inflation
Nitric Oxide Synthase
Prostaglandins
Nitric Oxide
Forearm
Muscles
Arterial Pressure
Brachial Artery
Drug and Narcotic Control
Vasodilation
Blood Vessels
Arginine
Dilatation
Pressure

Keywords

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

ASJC Scopus subject areas

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

Cite this

@article{21c0119cd26b44a4a75d58450028c41b,
title = "Prostaglandins do not contribute to the nitric oxide-mediated compensatoryvasodilation in hypoperfused exercising muscle",
abstract = "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 [N G-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.",
keywords = "Blood flow, Exercise, Hypoperfusion, Nitric oxide, Prostaglandins, Vasodilation",
author = "Casey, {Darren P.} and Joyner, {Michael Joseph}",
year = "2011",
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T1 - Prostaglandins do not contribute to the nitric oxide-mediated compensatoryvasodilation in hypoperfused exercising muscle

AU - Casey, Darren P.

AU - Joyner, Michael Joseph

PY - 2011/7

Y1 - 2011/7

N2 - 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 [N G-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.

AB - 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 [N G-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.

KW - Blood flow

KW - Exercise

KW - Hypoperfusion

KW - Nitric oxide

KW - Prostaglandins

KW - Vasodilation

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DO - 10.1152/ajpheart.00222.2011

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AN - SCOPUS:79959859899

VL - 301

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

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