Cardiovascular and sympathetic effects of nitric oxide inhibition at rest and during static exercise in humans

Détails

ID Serval
serval:BIB_954730D93D16
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Cardiovascular and sympathetic effects of nitric oxide inhibition at rest and during static exercise in humans
Périodique
Circulation
Auteur(s)
Owlya  R., Vollenweider  L., Trueb  L., Sartori  C., Lepori  M., Nicod  P., Scherrer  U.
ISSN
0009-7322 (Print)
Statut éditorial
Publié
Date de publication
12/1997
Volume
96
Numéro
11
Pages
3897-903
Notes
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Dec 2
Résumé
BACKGROUND: Nitric oxide (NO) regulates vascular tone and blood pressure, and studies in animals suggest that it does so, at least in part, by modulating sympathetic neural outflow. Loss of NO-induced vasodilator tone and restraint on sympathetic vasoconstrictor outflow could lead to exaggerated vasoconstrictor and pressor responses to physical stress in humans. METHODS AND RESULTS: To determine the role of NO in the modulation of central sympathetic outflow and vascular tone at rest and during a physical stress, we tested effects of systemic inhibition of NO synthase by N(G)-monomethyl-L-arginine (L-NMMA) infusion (a stereospecific inhibitor of NO synthase) on sympathetic nerve activity (microneurography), regional vascular resistance, and blood pressure at rest and during static handgrip. The major new findings are that (1) under resting conditions, L-NMMA infusion, which increased mean arterial pressure by approximately 10%, did not have any detectable effect on muscle sympathetic nerve activity, whereas a similar increase in arterial pressure evoked by phenylephrine infusion (an NO-independent vasoconstrictor) decreased the rate of sympathetic nerve firing by approximately 50%; (2) during static handgrip, the exercise-induced sympathetic nerve responses were preserved during L-NMMA infusion but markedly attenuated during phenylephrine infusion; and (3) the L-NMMA-induced loss of vasodilator tone did not result in exaggerated exercise-induced pressor and calf vasoconstrictor responses. CONCLUSIONS: These findings indicate that NO is involved in the central regulation of sympathetic outflow in humans and suggest that both neuronal and endothelial NO synthesis may contribute to the regulation of vasomotor tone.
Mots-clé
Adrenergic alpha-Agonists/diagnostic use Adult Blood Flow Velocity Blood Pressure/drug effects/*physiology Enzyme Inhibitors/diagnostic use Exercise/*physiology Forearm/blood supply Humans Male Nitric Oxide Synthase/*antagonists & inhibitors Phenylephrine/diagnostic use Reference Values Rest/*physiology Sympathetic Nervous System/*physiology Sympathomimetics/diagnostic use Vascular Resistance/drug effects/*physiology Vasoconstrictor Agents/diagnostic use omega-N-Methylarginine/diagnostic use
Pubmed
Web of science
Création de la notice
25/01/2008 15:00
Dernière modification de la notice
03/03/2018 19:39
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