TY - JOUR
T1 - Prostaglandins do not contribute to the nitric oxide-mediated compensatoryvasodilation in hypoperfused exercising muscle
AU - Casey, Darren P.
AU - Joyner, Michael J.
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 [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.
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 [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.
KW - Blood flow
KW - Exercise
KW - Hypoperfusion
KW - Nitric oxide
KW - Prostaglandins
KW - Vasodilation
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U2 - 10.1152/ajpheart.00222.2011
DO - 10.1152/ajpheart.00222.2011
M3 - Article
C2 - 21536852
AN - SCOPUS:79959859899
SN - 0363-6135
VL - 301
SP - H261-H268
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 1
ER -