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Evidence of the regulatory potential of human skeletal muscle feed arteries
Author(s) -
Ives Stephen James,
Andtbacka Robert Hans Ingemar,
Noyes R. Dirk,
Donato Anthony,
Park Song Young,
Gifford Jayson,
Lesniewski Lisa,
McCullagh Joseph,
Richardson Russell S
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.1138.29
Subject(s) - vasoconstriction , vasodilation , electrical impedance myography , phenylephrine , vascular resistance , sodium nitroprusside , medicine , vascular smooth muscle , endocrinology , skeletal muscle , blood vessel , chemistry , cardiology , anatomy , blood pressure , nitric oxide , smooth muscle
Prior work has documented the regulatory role of skeletal muscle feed arteries in rodent models, however it is unknown if human skeletal muscle feed arteries display such functionality. Feed arteries (888±188 μm ID) from 6 humans (53±3 yrs) were studied using pressure myography. Vessel function was assessed using potassium chloride (KCl), phenylephrine (PE), acetylcholine (ACh), and sodium nitroprusside (SNP) dose response curves (DRCs) to characterize non‐receptor and receptor‐mediated vasoconstriction as well as endothelium‐dependent and independent vasodilation, respectively. Vascular resistance was calculated using internal diameter changes due to pharmacological stimulation and Poiseuilles’ law (R= 8nL/πr 4 ). Vessel function protocols revealed robust vasoconstriction in response to PE and KCl (37 ± 6; 43 ± 19 % vasoconstriction, respectively), but also achieved significant vasodilation with ACh and SNP (97 ± 11; 117 ± 24 % vasodilation, respectively). Using the maximal PE and KCl‐induced vasoconstriction, vascular resistance was calculated to increase by 304 and 392%, respectively. These findings provide evidence that human skeletal muscle feed arteries are capable of generating significant changes in vascular resistance, and thus likely play a role in blood flow regulation. Support by NIH PO1 HL‐091830.