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Influence of Combined Nitric Oxide and Prostaglandin Inhibition on Contraction‐induced Rapid Vasodilation
Author(s) -
Kirby Brett S,
Tschakovsky Michael E,
Larson Dennis G,
Dinenno Frank A
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1108.13
Subject(s) - nitric oxide , contraction (grammar) , vasodilation , prostaglandin , chemistry , pharmacology , medicine , biochemistry
A monophasic increase in skeletal muscle blood flow is observed following a brief single forearm contraction in young healthy adults. The factors facilitating this rapid vasodilatory response are unclear. We tested the hypothesis that nitric oxide (NO) and prostaglandins (PGs) contribute to contraction‐induced rapid vasodilation in humans. We measured forearm blood flow (Doppler ultrasound) and calculated vascular conductance 10s prior to, and for 30s after a single 1‐s dynamic forearm contraction at mild and moderate exercise intensity. Trials were performed in eight young subjects before and after combined inhibition of NO and PG synthesis. For both workloads, the immediate and peak dilatory responses (cardiac cycles 1 – 4 P>0.05) were not influenced by combined inhibition, however the sustained dilation was blunted (cardiac cycles 5 – 23; P<0.05). The total hyperemic response to a single contraction was significantly attenuated at both mild and moderate contraction intensity (~70%). The present study indicates that NO and vasodilating PGs contribute to the latter sustained portion of the contraction‐induced rapid vasodilatory response. Our collective findings suggest that multiple vasoactive signals are likely acting in concert, and have a specific role in coordinating the magnitude and temporal pattern of contraction‐induced rapid vasodilation. Supported by HL‐095573