April 3, 2001Circulation
Role of Endothelial Nitric Oxide in Shear Stress–Induced Vasodilation of Human Microvasculature
Why the study?
Does shear stress induce NO-mediated vasodilation in human microvasculature, and is this mechanism altered in hypertension or hypercholesterolemia?
Population
32 subjects providing arteries isolated from gluteal fat biopsies.
Comparison
Shear stress induced by increasing flow rate… vs Normal controls vs hypertensive vs…
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Distinguishes NO-dependent impairment in hypertension from preserved non-NO responses in hypercholesterolemia; leaves open human translation.
Structured PICO
Does shear stress induce NO-mediated vasodilation in human microvasculature, and is this mechanism altered in hypertension or hypercholesterolemia?
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Population
32 subjects (9 normal controls, 11 hypertensive patients, and 12 hypercholesterolemic patients) providing arteries isolated from gluteal fat biopsies.
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Intervention
Shear stress induced by increasing flow rate from 1 to 50 microL/min after preconstriction with norepinephrine, with and without NO synthase inhibitor Nomega-nitro-L-arginine (L-NNA) or endothelial removal.
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Comparator
Normal controls vs hypertensive vs hypercholesterolemic patients; baseline flow vs increased flow; presence vs absence of L-NNA.
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Outcome
Flow-mediated vasodilation (arterial internal diameter expressed as percent of norepinephrine-induced constriction).surrogate
Shear stress induces endothelium-dependent, NO-mediated vasodilation in human microvasculature, which is impaired in hypertension but preserved via non-NO mechanisms in hypercholesterolemia.
Cite This Study
Paniagua et al. (2001) studied this question.