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Nitric oxide in the regulation of vasomotor tone in human skeletal muscle

Nitric oxide in the regulation of vasomotor tone in human skeletal muscle Abstract The role of nitric oxide (NO) as a regulator of vasomotor tone has been investigated in resting and exercising human skeletal muscle. At rest, NO synthase (NOS) inhibition by intra-arterial infusion of N G -monomethyl- l -arginine decreased femoral artery blood flow (FABF, ultrasound Doppler) from 0.39 ± 0.08 to 0.18 ± 0.03 l/min ( P < 0.01), i.e., by ∼52%, and increased leg O 2 extraction from 62.1 ± 9.8 to 100.9 ± 4.5 ml/l ( P < 0.004); thus leg O 2 uptake (V˙ o 2 , 22 ± 4 ml/min, ∼0.75 ml ⋅ min −1 ⋅ 100 g −1 ) was unaltered not significant ( P = NS). Mean arterial pressure (MAP) increased by 8 ± 2 mmHg ( P < 0.01). Heart rate (HR, 53 ± 3 beats/min) was unaltered ( P = NS). The NOS inhibition had, however, no effect on the initial rate of rise or the magnitude of FABF (4.8 ± 0.4 l/min, ∼163 ml ⋅ min −1 ⋅ 100 g −1 ), MAP (117 ± 3 mmHg), HR (98 ± 5 beats/min), or legV˙ o 2 (704 ± 55 ml/min, ∼24 ml ⋅ min −1 ⋅ 100 g −1 , P = NS) during submaximal, one-legged, dynamic knee-extensor exercise. Similarly, FABF (7.6 ± 1.0 l/min, ∼258 ml ⋅ min −1 ⋅ 100 g −1 ), MAP (140 ± 8 mmHg), and leg V˙ o 2 (1,173 ± 139 ml/min, ∼40 ml ⋅ min −1 ⋅ 100 g −1 ) were unaffected at termination of peak effort ( P = NS). Peak HR (137 ± 3 beats/min) was, however, lowered by 10% ( P < 0.01). During recovery, NOS inhibition reduced FABF by ∼34% ( P < 0.04), which was compensated for by an increase in the leg O 2 extraction by ∼41% ( P < 0.04); thus legV˙ o 2 was unaltered ( P = NS). In conclusion, these findings indicate that NO is not essential for the initiation or maintenance of active hyperemia in human skeletal muscle but support a role for NO during rest, including recovery from exercise. Moreover, changes in blood flow during rest and recovery caused by NOS inhibition are accompanied by reciprocal changes in O 2 extraction, and thusV˙ o 2 is maintained. blood flow circulation exercise metabolism vasodilatation Footnotes Address for reprint requests and other correspondence: G. Rådegran, Copenhagen Muscle Research Centre, Rigshospitalet, Sect. 7652, Tagensvej 20, DK-2200 Copenhagen N, Denmark (E-mail: goran@rh.dk ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. §1734 solely to indicate this fact. Copyright © 1999 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Nitric oxide in the regulation of vasomotor tone in human skeletal muscle

AJP - Heart and Circulatory Physiology , Volume 276 (6): H1951 – Jun 1, 1999

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
See Article on Publisher Site

Abstract

Abstract The role of nitric oxide (NO) as a regulator of vasomotor tone has been investigated in resting and exercising human skeletal muscle. At rest, NO synthase (NOS) inhibition by intra-arterial infusion of N G -monomethyl- l -arginine decreased femoral artery blood flow (FABF, ultrasound Doppler) from 0.39 ± 0.08 to 0.18 ± 0.03 l/min ( P < 0.01), i.e., by ∼52%, and increased leg O 2 extraction from 62.1 ± 9.8 to 100.9 ± 4.5 ml/l ( P < 0.004); thus leg O 2 uptake (V˙ o 2 , 22 ± 4 ml/min, ∼0.75 ml ⋅ min −1 ⋅ 100 g −1 ) was unaltered not significant ( P = NS). Mean arterial pressure (MAP) increased by 8 ± 2 mmHg ( P < 0.01). Heart rate (HR, 53 ± 3 beats/min) was unaltered ( P = NS). The NOS inhibition had, however, no effect on the initial rate of rise or the magnitude of FABF (4.8 ± 0.4 l/min, ∼163 ml ⋅ min −1 ⋅ 100 g −1 ), MAP (117 ± 3 mmHg), HR (98 ± 5 beats/min), or legV˙ o 2 (704 ± 55 ml/min, ∼24 ml ⋅ min −1 ⋅ 100 g −1 , P = NS) during submaximal, one-legged, dynamic knee-extensor exercise. Similarly, FABF (7.6 ± 1.0 l/min, ∼258 ml ⋅ min −1 ⋅ 100 g −1 ), MAP (140 ± 8 mmHg), and leg V˙ o 2 (1,173 ± 139 ml/min, ∼40 ml ⋅ min −1 ⋅ 100 g −1 ) were unaffected at termination of peak effort ( P = NS). Peak HR (137 ± 3 beats/min) was, however, lowered by 10% ( P < 0.01). During recovery, NOS inhibition reduced FABF by ∼34% ( P < 0.04), which was compensated for by an increase in the leg O 2 extraction by ∼41% ( P < 0.04); thus legV˙ o 2 was unaltered ( P = NS). In conclusion, these findings indicate that NO is not essential for the initiation or maintenance of active hyperemia in human skeletal muscle but support a role for NO during rest, including recovery from exercise. Moreover, changes in blood flow during rest and recovery caused by NOS inhibition are accompanied by reciprocal changes in O 2 extraction, and thusV˙ o 2 is maintained. blood flow circulation exercise metabolism vasodilatation Footnotes Address for reprint requests and other correspondence: G. Rådegran, Copenhagen Muscle Research Centre, Rigshospitalet, Sect. 7652, Tagensvej 20, DK-2200 Copenhagen N, Denmark (E-mail: goran@rh.dk ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. §1734 solely to indicate this fact. Copyright © 1999 the American Physiological Society

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Jun 1, 1999

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