TY - JOUR
T1 - Impact of aging on conduit artery retrograde and oscillatory shear at rest and during exercise
T2 - Role of nitric oxide
AU - Padilla, Jaume
AU - Simmons, Grant H.
AU - Fadel, Paul J.
AU - Laughlin, M. Harold
AU - Joyner, Michael J.
AU - Casey, Darren P.
PY - 2011/3
Y1 - 2011/3
N2 - 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-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 and 0.11±.0.02 arbitrary units, respectively) compared with young subjects (-4.8±2.3 s 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.
AB - 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-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 and 0.11±.0.02 arbitrary units, respectively) compared with young subjects (-4.8±2.3 s 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.
KW - age
KW - nitric oxide bioavailability
KW - oscillatory shear stress
KW - retrograde shear stress
KW - vascular conductance
UR - http://www.scopus.com/inward/record.url?scp=79953240729&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79953240729&partnerID=8YFLogxK
U2 - 10.1161/HYPERTENSIONAHA.110.165365
DO - 10.1161/HYPERTENSIONAHA.110.165365
M3 - Article
C2 - 21263118
AN - SCOPUS:79953240729
SN - 0194-911X
VL - 57
SP - 484
EP - 489
JO - Hypertension
JF - Hypertension
IS - 3
ER -