title: Cardiovascular and sympathetic effects of nitric oxide inhibition at rest and during static exercise in humans.
abstract: 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.
  
  
  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.
authors.affiliation: Department of Internal Medicine B, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
authors.forename: R
authors.initials: R
authors.lastname: Owlya
authors.forename: L
authors.initials: L
authors.lastname: Vollenweider
authors.forename: L
authors.initials: L
authors.lastname: Trueb
authors.forename: C
authors.initials: C
authors.lastname: Sartori
authors.forename: M
authors.initials: M
authors.lastname: Lepori
authors.forename: P
authors.initials: P
authors.lastname: Nicod
authors.forename: U
authors.initials: U
authors.lastname: Scherrer
mesh_terms: D000316:Adrenergic alpha-Agonists; D000328:Adult; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors; D015444:Exercise / Q000502:physiology*; D005542:Forearm / Q000098:blood supply; D006801:Humans; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D010656:Phenylephrine; D012016:Reference Values; D012146:Rest / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology*; D013566:Sympathomimetics; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents; D019323:omega-N-Methylarginine
chemical_list: D000316:Adrenergic alpha-Agonists; D004791:Enzyme Inhibitors; D013566:Sympathomimetics; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D019323:omega-N-Methylarginine; D019001:Nitric Oxide Synthase