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Vascular hyperpolarization contributes to onset and steady‐state exercise hyperemia in humans
Author(s) -
Crecelius Anne R.,
Kirby Brett S.,
Richards Jennifer C.,
Garcia Leora J.,
Luckasen Gary J.,
Larson Dennis G.,
Dinenno Frank A.
Publication year - 2012
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.26.1_supplement.1138.43
Subject(s) - hyperpolarization (physics) , vasodilation , medicine , ouabain , anesthesia , dilator , steady state (chemistry) , chemistry , endocrinology , cardiology , sodium , organic chemistry , nuclear magnetic resonance spectroscopy
We tested the hypothesis that vascular hyperpolarization contributes to both the onset and steady‐state hyperemic response to exercise. In Protocol 1 (n=11), forearm blood flow (FBF; Doppler ultrasound) was measured during rhythmic handgrip exercise at 10% maximal voluntary contraction for 5 minutes under control (intra‐arterial saline; T1) conditions, after combined inhibition of Na + /K + ATPase and K IR channels [via ouabain and barium chloride (BaCl 2 ), respectively; T2] alone and in the presence of combined nitric oxide synthase (L‐NMMA) and cyclooxygenase inhibition (ketorolac; T3). Drugs were not infused during exercise due to potential influences on basal vascular tone. The total hyperemic responses were significantly ( P <0.05) attenuated from control at 30 seconds (50 ± 4 and 65 ± 2%), 1 minute (34 ± 4 and 41 ± 3%), and 2 minutes (20 ± 4 and 23 ± 4%; T2 and T3 respectively) of exercise. FBF was not different in the last 2 minutes of exercise. In Protocol 2 (n=6), all study drugs were infused prior to and during exercise to assess the impact on steady‐state hyperemia. Steady‐state FBF was significantly reduced during T2 vs T1 (123 ± 18 vs 156 ± 21 ml/min; −21 ± 4%), and further reduced during T3 (108 ± 17 ml/min; −32 ± 3%). Our data indicate vascular hyperpolarization as a novel contributing vasodilatory pathway in the complex blood flow response to exercise at the onset and during steady‐state hyperemia. Supported by HL102720