Passive leg movement and nitric oxide-mediated vascular function: the impact of age

In young healthy men, passive leg movement (PLM) elicits a robust nitric oxide (NO)-dependent increase in leg blood flow (LBF), thus providing a novel approach to assess NO-mediated vascular function. While the magnitude of the LBF response to PLM is markedly reduced with age, the role of NO in this...

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Veröffentlicht in:American Journal of Physiology: Cell Physiology 2015-03, Vol.308 (6), p.H672-H679
Hauptverfasser: Trinity, Joel D, Groot, H Jonathan, Layec, Gwenael, Rossman, Matthew J, Ives, Stephen J, Morgan, David E, Gmelch, Ben S, Bledsoe, Amber, Richardson, Russell S
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container_end_page H679
container_issue 6
container_start_page H672
container_title American Journal of Physiology: Cell Physiology
container_volume 308
creator Trinity, Joel D
Groot, H Jonathan
Layec, Gwenael
Rossman, Matthew J
Ives, Stephen J
Morgan, David E
Gmelch, Ben S
Bledsoe, Amber
Richardson, Russell S
description In young healthy men, passive leg movement (PLM) elicits a robust nitric oxide (NO)-dependent increase in leg blood flow (LBF), thus providing a novel approach to assess NO-mediated vascular function. While the magnitude of the LBF response to PLM is markedly reduced with age, the role of NO in this attenuated response in the elderly is unknown. Therefore, this study sought to determine the contribution of NO in the PLM-induced LBF with age. Fourteen male subjects (7 young, 24 ± 1 yr; and 7 old, 75 ± 3 yr) underwent PLM with and without NO synthase (NOS) inhibition achieved by intra-arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA). LBF was determined second-by-second by Doppler ultrasound, and central hemodynamics were measured by finger photoplethysmography. NOS inhibition blunted the PLM-induced peak increase in LBF in the young (control: 668 ± 106; 431 ± 95 Δml/min; P = 0.03) but had no effect in the old (control: 266 ± 98; 251 ± 92 Δml/min; P = 0.59). Likewise, the magnitude of the reduction in the overall (i.e., area under the curve) PLM-induced LBF response to NOS inhibition was less in the old (LBF: -31 ± 18 ml) than the young (LBF: -129 ± 21 ml; P < 0.01). These findings suggest that the age-associated reduction in PLM-induced LBF in the elderly is primarily due to a reduced contribution to vasodilation from NO and therefore support the use of PLM as a novel approach to assess NO-mediated vascular function across the lifespan.
doi_str_mv 10.1152/ajpheart.00806.2014
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While the magnitude of the LBF response to PLM is markedly reduced with age, the role of NO in this attenuated response in the elderly is unknown. Therefore, this study sought to determine the contribution of NO in the PLM-induced LBF with age. Fourteen male subjects (7 young, 24 ± 1 yr; and 7 old, 75 ± 3 yr) underwent PLM with and without NO synthase (NOS) inhibition achieved by intra-arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA). LBF was determined second-by-second by Doppler ultrasound, and central hemodynamics were measured by finger photoplethysmography. NOS inhibition blunted the PLM-induced peak increase in LBF in the young (control: 668 ± 106; 431 ± 95 Δml/min; P = 0.03) but had no effect in the old (control: 266 ± 98; 251 ± 92 Δml/min; P = 0.59). Likewise, the magnitude of the reduction in the overall (i.e., area under the curve) PLM-induced LBF response to NOS inhibition was less in the old (LBF: -31 ± 18 ml) than the young (LBF: -129 ± 21 ml; P &lt; 0.01). These findings suggest that the age-associated reduction in PLM-induced LBF in the elderly is primarily due to a reduced contribution to vasodilation from NO and therefore support the use of PLM as a novel approach to assess NO-mediated vascular function across the lifespan.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>25576629</pmid><doi>10.1152/ajpheart.00806.2014</doi><oa>free_for_read</oa></addata></record>
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subjects Adult
Age
Age Factors
Aged
Arterial Pressure
Blood Flow Velocity
Cardiovascular system
Enzyme Inhibitors - administration & dosage
Femoral Artery - diagnostic imaging
Femoral Artery - metabolism
Heart Rate
Humans
Impact analysis
Infusions, Intra-Arterial
Integrative Cardiovascular Physiology and Pathophysiology
Legs
Lower Extremity
Male
Movement
Muscle Contraction
Muscle, Skeletal - blood supply
Muscle, Skeletal - metabolism
Nitric oxide
Nitric Oxide - metabolism
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - metabolism
omega-N-Methylarginine - administration & dosage
Regional Blood Flow
Stroke Volume
Ultrasonography
Vasodilation - drug effects
Young Adult
title Passive leg movement and nitric oxide-mediated vascular function: the impact of age
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