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Contribution of nitric oxide to the blood pressure and arterial responses to exercise in humans
Citation
Campbell, R and Fisher, JP and Sharman, JE and McDonnell, BJ and Frenneaux, MP, Contribution of nitric oxide to the blood pressure and arterial responses to exercise in humans , Journal of Human Hypertension, 25 pp. 262-270. ISSN 0950-9240 (2011) [Refereed Article]
Copyright Statement
Copyright © 2010 Nature Publishing Group
Official URL: http://www.nature.com/jhh/journal/vaop/ncurrent/fu...
Abstract
An exaggerated blood pressure (BP) response to
exercise predicts future cardiovascular risk. The mechanisms
underlying exercise-induced hypertension
remain unclear, although endothelial dysfunction and
elevated arterial stiffness may contribute. Given the
association between reductions in nitric oxide (NO) and
vascular dysfunction, we sought to determine whether
acute inhibition of NO synthase with NG-monomethyl-Larginine
(L-NMMA) would lead to exaggerated BP
responses to maximal exercise and attenuate exerciseinduced
reductions in arterial stiffness. In 10 healthy
subjects (31±5 years), BP and heart rate (HR) were
measured before, during and after an incremental
cycling exercise test to determine maximal oxygen
consumption (VO2max). Trials were performed with
placebo (saline) or intravenous infusion of L-NMMA on
separate days in a randomized, double-blind, crossover
design. Central (aortic) and peripheral (femoral) arterial
stiffness were assessed using pulse wave velocity
(PWV). BP was increased with L-NMMA at rest and
during sub-maximal exercise, but not at maximal
exercise (mean BP 117±5 vs 118±8mmHg, saline vs
L-NMMA, P40.05). Furthermore, L-NMMA had no influence
on exercising HR or VO2max (P>0.05). Notably,
aortic PWV was similarly increased after exercise with
either saline or L-NMMA (P<0.05), whereas postexercise
decreases in femoral PWV were attenuated with L-NMMA
(P<0.05). Our findings suggest that NO is an important
contributor to reductions in femoral artery stiffness after
maximal exercise in healthy individuals. Furthermore,
acute pharmacological inhibition of NO synthase causes
augmented BP responses to sub-maximal exercise, but
does not lead to exaggerated BP responses to maximal
exercise or reduce maximal oxygen consumption.
Item Details
Item Type: | Refereed Article |
---|---|
Keywords: | blood pressure; exercise; nitric oxide; arteries; vasculature |
Research Division: | Biomedical and Clinical Sciences |
Research Group: | Cardiovascular medicine and haematology |
Research Field: | Cardiology (incl. cardiovascular diseases) |
Objective Division: | Health |
Objective Group: | Clinical health |
Objective Field: | Clinical health not elsewhere classified |
UTAS Author: | Sharman, JE (Professor James Sharman) |
ID Code: | 66350 |
Year Published: | 2011 |
Web of Science® Times Cited: | 31 |
Deposited By: | Menzies Institute for Medical Research |
Deposited On: | 2011-01-13 |
Last Modified: | 2013-11-15 |
Downloads: | 0 |
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