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Augmentation of Functional Sympatholysis via Endothelial Signaling Is Independent of Nitric Oxide and Prostaglandins in Humans
Author(s) -
Hearon Christopher,
Kirby Brett,
Crecelius Anne,
Luckasen Gary,
Larson Dennis,
Dinenno Frank
Publication year - 2015
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.29.1_supplement.649.9
Subject(s) - vasoconstriction , vasodilation , nitric oxide , medicine , dilator , endothelium , endocrinology , endothelial dysfunction , acetylcholine , anesthesia , chemistry
Sympathetic vasoconstriction is blunted in contracting skeletal muscle in an intensity dependent manner, and increasing endothelium‐dependent vasodilatory signaling during mild exercise can augment this “sympatholysis” similar to that observed during moderate exercise. Here, we determine the role of nitric oxide (NO) and vasodilating prostaglandins (PGs) to the endothelium‐dependent augmentation of sympatholysis during mild exercise. In 10 young subjects we measured forearm blood flow (Doppler ultrasound) and calculated vascular conductance (FVC) responses to local intra‐arterial infusion of phenylephrine (PE; α1‐agonist) during 1) infusion of the endothelium‐dependent dilator acetylcholine (ACH), 2) moderate (15% maximum voluntary contraction; MVC) handgrip exercise and 3) mild (5% MVC) exercise + ACH infusion. Trials were repeated after combined local blockade of NO/PGs (L‐NMMA/Ketorolac, respectively). Vasoconstriction to PE was blunted during 15% exercise compared to control ACH infusion (ΔFVC: ‐14±3% vs ‐30±3%, P<0.05). Augmenting endothelium‐dependent signaling during 5% exercise blunted vasoconstriction similar to 15% exercise (ΔFVC: ‐8±4%). After blockade of NO/PGs, vasoconstriction to PE was blunted in all conditions (ΔFVC: ACH: ‐20±5%; 15% MVC: ‐15±5%; 5%MVC + ACH: ‐7±4%; all P<0.05) relative to control ACH infusion. These data demonstrate that increasing endothelial vasodilatory signaling limits sympathetic vasoconstriction independent of NO/PGs, implicating a role for endothelial hyperpolarization in sympatholysis in humans. Support: HL102720