期刊
HYPERTENSION
卷 57, 期 3, 页码 484-489出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.110.165365
关键词
age; retrograde shear stress; oscillatory shear stress; nitric oxide bioavailability; vascular conductance
资金
- NIH [AR-55819, HL-46493, CTSA RR-024150, HL-093167, T32-AR048523]
- Mayo Foundation
Aging has been recently associated with increased retrograde and oscillatory shear in peripheral conduit arteries, a hemodynamic environment that favors a proatherogenic endothelial cell phenotype. We evaluated whether nitric oxide (NO) bioavailability in resistance vessels contributes to age-related differences in shear rate patterns in upstream conduit arteries at rest and during rhythmic muscle contraction. Younger (n=11, age 26 +/- 2 years) and older (n=11, age 61 +/- 2 years) healthy subjects received intra-arterial saline (control) and the NO synthase inhibitor N-G-Monomethyl-L-arginine. Brachial artery diameter and velocities were measured via Doppler ultrasound at rest and during a 5-minute bout of rhythmic forearm exercise. At rest, older subjects exhibited greater brachial artery retrograde and oscillatory shear (-13.2 +/- 3.0 s(-1) and 0.11 +/-.0.02 arbitrary units, respectively) compared with young subjects (-4.8 +/- 2.3 s(-1) and 0.04 +/- 0.02 arbitrary units, respectively; both P < 0.05). NO synthase inhibition in the forearm circulation of young, but not of older, subjects increased retrograde and oscillatory shear (both P < 0.05), such that differences between young and old at rest were abolished (both P>0.05). From rest to steady-state exercise, older subjects decreased retrograde and oscillatory shear (both P < 0.05) to the extent that no exercise-related differences were found between groups (both P > 0.05). Inhibition of NO synthase in the forearm circulation did not affect retrograde and oscillatory shear during exercise in either group (all P > 0.05). These data demonstrate for the first time that reduced NO bioavailability in the resistance vessels contributes, in part, to age-related discrepancies in resting shear patterns, thus identifying a potential mechanism for increased risk of atherosclerotic disease in conduit arteries. (Hypertension. 2011;57:484-489.)
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